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.


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
B.S. Exercise Science
University of Delaware, Newark, DE
Concentration: Exercise Physiology
Minor: Biological Sciences


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

Professional Memberships

American College of Sports Medicine (ACSM)
American Physiological Society (APS)
American Heart Association (AHA)
Gerontological Society of America (GSA)
American Society of Nephrology (ASN)

Honors & Awards

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

Extramural Funding

  • 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
  • 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
  • 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

LaRocca TJ, Martens CR, Seals DR. Nutrition and other lifestyle influences on arterial aging. Ageing Res Rev. 2016. S1568-1637(16)30227-6.


As our world's population ages, cardiovascular diseases (CVD) will become an increasingly urgent public health problem. A key antecedent to clinical CVD and many other chronic disorders of aging is age-related arterial dysfunction, characterized by increased arterial stiffness and impaired arterial endothelial function. Accumulating evidence demonstrates that diet and nutrition may favorably modulate these arterial functions with aging, but many important questions remain. In this review, we will summarize the available information on dietary patterns and nutritional factors that have been studied for their potential to reduce arterial stiffness and improve endothelial function with age, with an emphasis on: 1) underlying physiological mechanisms, and 2) emerging areas of research on nutrition and arterial aging that may hold promise for preventing age-related CVD.

Martens CR, Seals DR. Practical alternatives to chronic caloric restriction for optimizing vascular function with aging. J Physiol. 2016. ePub Ahead of Print.


Calorie restriction (CR) in the absence of malnutrition exerts a multitude of physiological benefits with aging in model organisms and in humans including improvements in vascular function. Despite the well-known benefits of chronic CR, long-term energy restriction is likely not a feasible healthy lifestyle strategy in humans due to poor sustained adherence, and presents additional concerns if applied to normal weight older adults. The purpose of this review will be to summarize what is known about the effects of CR on vascular function with aging including the underlying molecular "energy- and nutrient-sensing" mechanisms, and to discuss the limited but encouraging evidence for alternative pharmacological and lifestyle interventions that may improve vascular function with aging by mimicking the beneficial effects of long-term CR.

de Picciotto NE, Gano LB, Johnson LC, Martens CR, Sindler AL, Mills KF, Imai SI, Seals DR. Nicotinamide mononucleotide supplementation reverses vascular dysfunction and oxidative stress with aging in mice. Aging Cell. 2016. ePub Ahead of Print.


We tested the hypothesis that supplementation of nicotinamide mononucleotide (NMN), a key NAD+ intermediate, increases arterial SIRT1 activity and reverses age-associated arterial dysfunction and oxidative stress. Old control mice (OC) had impaired carotid artery endothelium-dependent dilation (EDD) (60 ± 5% vs. 84 ± 2%), a measure of endothelial function, and nitric oxide (NO)-mediated EDD (37 ± 4% vs. 66 ± 6%), compared with young mice (YC). This age-associated impairment in EDD was restored in OC by the superoxide (O2-) scavenger TEMPOL (82 ± 7%). OC also had increased aortic pulse wave velocity (aPWV, 464 ± 31 cm s-1 vs. 337 ± 3 cm s-1 ) and elastic modulus (EM, 6407 ± 876 kPa vs. 3119 ± 471 kPa), measures of large elastic artery stiffness, compared with YC. OC had greater aortic O2- production (2.0 ± 0.1 vs. 1.0 ± 0.1 AU), nitrotyrosine abundance (a marker of oxidative stress), and collagen-I, and reduced elastin and vascular SIRT1 activity, measured by the acetylation status of the p65 subunit of NFκB, compared with YC. Supplementation with NMN in old mice restored EDD (86 ± 2%) and NO-mediated EDD (61 ± 5%), reduced aPWV (359 ± 14 cm s-1 ) and EM (3694 ± 315 kPa), normalized O2- production (0.9 ± 0.1 AU), decreased nitrotyrosine, reversed collagen-I, increased elastin, and restored vascular SIRT1 activity. Acute NMN incubation in isolated aortas increased NAD+ threefold and manganese superoxide dismutase (MnSOD) by 50%. NMN supplementation may represent a novel therapy to restore SIRT1 activity and reverse age-related arterial dysfunction by decreasing oxidative stress.

Martens CR, Kirkman DL, Edwards DG. The Vascular Endothelium in Chronic Kidney Disease: A Novel Target for Aerobic Exercise. Exerc Sport Sci Rev. 2016. 44(1):12-9.


Endothelial dysfunction occurs in chronic kidney disease (CKD) and increases the risk for cardiovascular disease. The mechanisms of endothelial dysfunction seem to evolve throughout kidney disease progression, culminating in reduced L-arginine transport and impaired nitric oxide bioavailability in advanced disease. This review examines the hypothesis that aerobic exercise may reverse endothelial dysfunction by improving endothelial cell L-arginine uptake in CKD.

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.


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.


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 ⅚ 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-[(3)H]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.


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 H(2)O(2) 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.


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 dysfunction in chronic kidney disease. Cardiol Res Pract. 2011. 2011:267257.


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.