Sport and Exercise Science
University of Northern Colorado
Type of Resources
Place of Publication
University of Northern Colorado
Otto Warburg, a German physiologist, deduced that cancer cells exhibit a remarkably different metabolic profile in comparison to normal healthy cells characterized by increased rates of glycolysis and lactate fermentation, even in the presence of adequate oxygen content. Through the respective gain of function/loss of function of oncogenes and tumor suppressor genes, three major genes emerge as hallmarks of carcinogenic metabolic reconfiguration; HIF-1a, c-Myc oncogenes, and p53 tumor-suppressor genes. A result of their respective gain/loss of function are the upregulation of several glycolytic proteins and subsequent high rates of glucose influx into the tumor microenvironment, as well as lactate production, accumulation, and extrusion out of the tumor microenvironment. Patterns of lactate accumulation in apparently healthy models upon a progressive exercise bout before and after an exercise intervention exist in the structure of Resting, Lactate Thresholds 1 & 2 (LT1/LT2), Onset of Blood Lactate Accumulation (OBLA), and Peak parameters. However, it is unclear how the structure of these parameters applies to a cancer population and further, between cancer survivors actively receiving cancer therapy and cancer survivors who are not. Purpose: To investigate blood lactate accumulation response to a progressive exercise bout to volitional fatigue before and after a 12-week exercise-based oncology rehabilitation intervention between active and inactive cancer survivors. Methods: 21 cancer survivors (active, n=7; inactive, n=14) were invited to participate in a 12 week exercise-based oncology rehabilitation program at the University of Northern Colorado Cancer Rehabilitation Institute. All participants performed an initial assessment consisting of several physiological parameters, including body composition, pulmonary function, balance, muscular strength, muscular endurance, cardiovascular fitness, and lactate accumulation (LA). LA was quantified every 2 minutes during a progressive treadmill protocol to volitional fatigue via finger stick. The 12-week exercise intervention consisted of one-hour exercise sessions with trained Cancer Exercise Specialists focusing on cardiovascular endurance, muscular strength and endurance, balance, and flexibility exercises. Following the 12 week-exercise based intervention, participants completed a reassessment of the same physiological parameters. Results: Resting, Peak, and METS at OBLA values of active and inactive cancer survivors before and after an exercise intervention were not different (P>0.05). Furthermore, Resting lactate, Peak lactate, and METS at OBLA values between active and inactive cancer survivors before and after an exercise intervention were insignificantly different (P>0.05). However, both METS at OBLA in both active and inactive survivors were significantly different before and after a 12-week exercise intervention (P<0.05). Conclusions: These findings may indicate similar responses of lactate handling to exercise training in both active and inactive cancer survivors. This outcome is supported by significance of increased METS at OBLA of the total subject population before and after a 12-week exercise intervention indicating an improved ability to buffer lactate at higher intensities during the UNCCRI treadmill protocol.
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