Ralph S. Paffenbarger Jr., Jeremy N. Morris, William L. Haskell, Paul D. Thompson and I-Min Lee
Amanda L. Zaleski, Linda S. Pescatello, Kevin D. Ballard, Gregory A. Panza, William Adams, Yuri Hosokawa, Paul D. Thompson and Beth A. Taylor
Context: Compression socks have become increasingly popular with athletes due to perceived enhancement of exercise performance and recovery. However, research examining the efficacy of compression socks to reduce exercise-associated muscle damage has been equivocal, with few direct measurements of markers of muscle damage. Objective: To examine the influence of compression socks worn during a marathon on creatine kinase (CK) levels. Design: A randomized controlled trial. Setting: 2013 Hartford Marathon, Hartford, CT. Participants: Adults (n = 20) randomized to control (CONTROL; n = 10) or compression sock (SOCK; n = 10) groups. Main Outcome Measures: Blood samples were collected 24 hours before, immediately after, and 24 hours following the marathon for the analysis of CK, a marker of muscle damage. Results: Baseline CK levels did not differ between CONTROL (89.3 [41.2] U/L) and SOCK (100.0 [56.2] U/L) (P = .63). Immediately following the marathon (≤1 h), CK increased 273% from baseline (P < .001 for time), with no difference in exercise-induced changes in CK from baseline between CONTROL (+293.9 [278.2] U/L) and SOCK (+233.1 [225.3] U/L; P = .60 for time × group). The day following the marathon (≤24 h), CK further increased 1094% from baseline (P < .001 for time), with no difference in changes in CK from baseline between CONTROL (+ 1191.9 [1194.8] U/L) and SOCK (+889.1 [760.2] U/L; P = .53 for time × group). These similar trends persisted despite controlling for potential covariates such as age, body mass index, and race finishing time (Ps > .29). Conclusions: Compression socks worn during a marathon do not appear to mitigate objectively measured markers of muscle damage immediately following and 24 hours after a marathon.
Joshua Lowndes, Robert F. Zoeller, George A. Kyriazis, Mary P. Miles, Richard L. Seip, Niall M. Moyna, Paul S. Visich, Linda S. Pescatello, Paul M. Gordon, Paul D. Thompson and Theodore J. Angelopoulos
The purpose of this study was to examine whether leptin levels affect the response of leptin to exercise training (ET) and whether this is also affected by C-reactive protein (CRP) or the three common Apolipoprotein E genotypes (APOE). Ninety-seven (male = 45, female = 52) sedentary individuals underwent 6 months of supervised ET. Blood was sampled before the initiation of ET, and again 24 and 72 hr after completion of the final training session. ET resulted in a small reduction in body mass (80.47 ± 18.03 vs 79.42 ± 17.34 kg, p < .01). Leptin was reduced 24 hr after the final exercise session (p < .01), but returned to normal after 72 hr (p > .05)—Pre: 13.51 ± 12.27, 24hr: 12.14 ± 12.34, 72hr: 12.98 ± 11.40 ng/ml. The most hyperleptinemic individuals had a greater initial response, which was sustained through to 72 hr after the final session in the pooled study population (p < .01), and in both males (p < .05) and females (p < .05) separately. CRP was related to leptin independently of body weight and positively related to the reductions in leptin. APOE genotype was not related to leptin levels and did not affect the response to ET. Leptin levels may only be reduced by ET in those with hyperleptinemia. In addition, both the initial extent of hyperleptinemia and the subsequent reduction in leptin may be related to low grade chronic systemic inflammation.
Amanda Zaleski, Beth Taylor, Braden Armstrong, Michael Puglisi, Priscilla Clarkson, Stuart Chipkin, Charles Michael White, Paul D. Thompson and Linda S. Pescatello
Insufficient 25-hydroxyvitamin D [25(OH)D] levels are associated with high resting blood pressure (BP). However, the relationship between 25(OH)D and the peak systolic BP (SBP) response to exercise, a predictor of future hypertension, has yet to be investigated. We sought to examine the relationship among serum 25(OH)D and the peak SBP response to a graded exercise stress test (GEST) among a large sample (n = 417) of healthy men (49%) and women (51%) over a broad age range (20–76 years; mean age: 44.1 ± 0.8 years). We hypothesized that individuals with clinically insufficient 25(OH)D would have a greater peak SBP response to a GEST compared to individuals with sufficient 25(OH)D levels. Fasting serum 25(OH)D, anthropometrics, resting BP, and peak exercise SBP were obtained at the baseline visit of a larger clinical trial (STOMP; NCT01140308). Mean 25(OH)D levels were 36.1 ± 0.7 ng/ml, with ∼35% of individuals classified as insufficient (<30 ng/ml). Average resting BP was 119 ± 13 mmHg/75 ± 10 mmHg, with 52.3% considered to have normal BP, while 25.2% had elevated BP and 22.5% had established hypertension. The peak SBP response to a GEST was similar between individuals with sufficient (48 ± 19 mmHg) versus insufficient (48 ± 18 mmHg) 25(OH)D (p = 1.000). One unexpected finding emerged such that individuals with sufficient 25(OH)D had higher resting SBP (120 ± 14 mmHg vs. 117 ± 13 mmHg; p = .020) than individuals with insufficient 25(OH)D. In contrast to our hypothesis, 25(OH)D levels were not associated with the peak SBP response to a GEST. Baseline 25(OH)D levels were positively correlated with resting SBP; however, the magnitude of this effect is likely not clinically meaningful.