PurposeThe aim of this study was to examine the physical and training characteristics of recreational marathon runners within finish time bandings (2.5–3 h, 3–3.5 h, 3.5–4 h, 4–4.5 h and >4.5 h).Materials and methodsA total of 97 recreational marathon runners (age 42.4 ± 9.9 years; mass 69.2 ± 11.3 kg; stature 172.8 ± 9.1 cm), with a marathon finish time of 229.1 ± 48.7 min, of whom n = 34 were female and n = 63 were male, completed an incremental treadmill test for the determination of lactate threshold (LT1), lactate turn point (LT2) and running economy (RE). Following a 7-min recovery, they completed a test to volitional exhaustion starting at LT2 for the assessment of trueV˙normalO2max. In addition, all participants completed a questionnaire gathering information on their current training regimes exploring weekly distances, training frequencies, types of sessions, longest run in a week, with estimations of training speed, and load and volume derived from these data.ResultsTraining frequency was shown to be significantly greater for the 2.5–3 h group compared to the 3.5–4 h runners (P < 0.001) and >4.5 h group (P = 0.004), while distance per session (km·session−1) was significantly greater for the 2.5–3 h group (16.1 ± 4.2) compared to the 3.5–4 h group (15.5 ± 5.2; P = 0.01) and >4.5 h group (10.3 ± 2.6; P = 0.001). Race speed correlated with LT1 (r = 0.791), LT2 (r = 0.721) and distance per session (r = 0.563).ConclusionThe data highlight profound differences for key components of marathon running (trueV˙normalO2max, LT1, LT2, RE and % trueV˙normalO2max) within a group of recreational runners with the discriminating training variables being training frequency and the absolute training speed.

Breast cancer (BC) prognosis in patients with type 2 diabetes mellitus (T2DM) was never investigated from the perspective of their DM therapy. Further exploration is needed as our data evaluating 248 DM patients with newly diagnosed BC (1997-2006) show an increase in cancer-related mortality associated with use of insulin (I) or insulin secretagogues (IS) after 30 months median follow-up. The hazard ratio (HR) of a recurrence-free event among BC patients receiving IS only compared to those treated with only non-secretagogues (NS) was 2.6 in a Cox model analysis (table 1). Presented data were adjusted for collaborative stage, estrogen receptor status, age and race. Disease-free survival was measured by cancer recurrence or death from any cause. These findings provide support for our hypothesis that use of I or IS for T2DM management in BC patients may lead to worsening of their cancer disease. Still, additional data investigating the extent of the insulin resistance and overall inflammation is needed. We aimed to measure a panel of biomarkers related to inflammation and insulin resistance and to investigate whether the profiles identified for cases receiving NS drugs are associated with a better BC prognosis as compared to cases receiving I or IS for T2DM therapy. Proposed study will be conducted on 70 T2DM+BC and respectively 140 comorbidity-matched BC women, all previously enrolled in our retrospective study and being donors in the DataBank and BioRepository program. Serum biomarker profiles will be analyzed by multivariate modeling using log-rank or Cox proportional hazards regression to detect differences in disease-free survival and mortality. We speculate that guiding T2DM therapy based on the baseline biomarker profile has the potential to improve recurrence and survival in BC patients. Findings consistent with this hypothesis will have direct and immediate applicability in BC care as screening and clinical intervention can be easily implemented.Table 1.Recurrence-free, disease-free, and overall mortality by Type II diabetes medication useMedication useNo. of eventsNo. at riskRecurrence-free survival aHR (95% CI)No. of eventsNo. at riskDisease-free free survival bHR (95% CI)No. of eventsNo. at riskOverall Mortality HR (95% CI)Non-secretagoguesNo974Ref1674Ref1475RefYes111700.53301700.83271710.91   (0.21, 1.30)  (0.44, 1.55)  (0.47, 1.79)Insulin secretagoguesNo8128Ref27128Ref24129RefYes121161.41191160.76171170.69   (0.54, 3.64)  (0.40, 1.44)  (0.35, 1.37)Non-secretagogues only585Ref1485Ref1285RefSecretagogues only6372.609372.297371.45   (0.63, 10.73)  (0.78, 6.73)  (0.44, 4.81)InsulinNo15188Ref31188Ref27189RefYes5561.1715561.4914571.61   (0.41, 3.30)  (0.80, 2.80)  (0.83, 3.12)Drug ClassesNone+NS only699Ref1799Ref1599Ref         S only6372.719371.637371.18   (0.78, 9.52)  (0.66, 4.05)  (0.43, 3.30)S+NS3520.805520.585530.64   (0.19, 3.33)  (0.21, 1.63)  (0.22, 1.85)I+/−SorNS5561.3915561.4714571.50   (0.41, 4.66)  (0.72, 2.99)  (0.71, 3.18) Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr LB-421.