Louise M. Burke and Mary P. Miles
Eric S. Rawson, Mary P. Miles, and D. Enette Larson-Meyer
Some dietary supplements are recommended to athletes based on data that supports improved exercise performance. Other dietary supplements are not ergogenic per se, but may improve health, adaptation to exercise, or recovery from injury, and so could help athletes to train and/or compete more effectively. In this review, we describe several dietary supplements that may improve health, exercise adaptation, or recovery. Creatine monohydrate may improve recovery from and adaptation to intense training, recovery from periods of injury with extreme inactivity, cognitive processing, and reduce severity of or enhance recovery from mild traumatic brain injury (mTBI). Omega 3-fatty acid supplementation may also reduce severity of or enhance recovery from mTBI. Replenishment of vitamin D insufficiency or deficiency will likely improve some aspects of immune, bone, and muscle health. Probiotic supplementation can reduce the incidence, duration, and severity of upper respiratory tract infection, which may indirectly improve training or competitive performance. Preliminary data show that gelatin and/or collagen may improve connective tissue health. Some anti-inflammatory supplements, such as curcumin or tart cherry juice, may reduce inflammation and possibly delayed onset muscle soreness (DOMS). Beta-hydroxy beta-methylbutyrate (HMB) does not consistently increase strength and/or lean mass or reduce markers of muscle damage, but more research on recovery from injury that includes periods of extreme inactivity is needed. Several dietary supplements, including creatine monohydrate, omega 3-fatty acids, vitamin D, probiotics, gelatin, and curcumin/tart cherry juice could help athletes train and/or compete more effectively.
Mary P. Miles, Erin E. Walker, Stephen B. Conant, Shelly P. Hogan, and Jessy R. Kidd
Attenuation of exercise-induced interleukin-6 (IL-6) responses by carbohydrate (CHO) has been demonstrated in studies comparing controlled doses (≥ 0.9 g · kg−1 · h−1) to placebo, but not in studies of voluntary intake. This study sought to determine if attenuation of the IL-6 response during a 32.2-km mountain trail race occurs for high compared to low ad libitum CHO intakes. IL-6, C-reactive protein (CRP), and creatine kinase activity (CK) were analyzed from blood samples collected 12 h pre-, 0, 4, and 24 h post-race. Subjects were grouped into low (n = 14, 0.4 ± 0.1 g · kg−1· h−1) and high (n = 18, 0.8 ± 0.2 g · kg−1 · h−1) CHO intake groups. IL-6 0 h post-race (P < 0.05) was higher in the low (40.2 ± 22.7 pg · mL−1) compared to the high CHO group (32.7 ± 22.1 pg · mL−1). CRP and CK both increased post-race, but no differences were observed between groups. Attenuation of exercise-induced IL-6 is apparent across a range of CHO intakes.
Rochelle D. Kirwan, Lindsay K. Kordick, Shane McFarland, Denver Lancaster, Kristine Clark, and Mary P. Miles
The purpose of this study was to determine the dietary, anthropometric, blood-lipid, and performance patterns of university-level American football players attempting to increase body mass during 8 wk of training.
Three-day diet records, body composition (DEXA scan), blood lipids, and performance measures were collected in redshirt football players (N = 15, age 18.5 ± 0.6 yr) early season and after 8 wk of in-season training.
There was an increase (p < .05) from early-season to postseason testing for reported energy (+45%), carbohydrate (+82%), and protein (+29%) intakes and no change in the intake of fat. Fat intake was 41% of energy at the early-season test and 32% of energy at the postseason test. Increases (p < .05 for all) in performance measures, lean mass (70.5 ± 7.7–71.8 ± 7.7 kg), fat mass (15.9 ± 6.2–17.3 ± 6.8 kg), plasma total cholesterol (193.5 ± 32.4–222.6 ± 40.0 mg/dl), and low-density lipoproteins (LDL; 92.7 ± 32.7–124.5 ± 34.7 mg/dl) were measured. No changes were measured in triglycerides, very-low-density lipoproteins, or high-density lipoproteins.
Increases in strength, power, speed, total body mass, muscle mass, and fat mass were measured. Cholesterol and LDL levels increased during the study to levels associated with higher risk for cardiovascular disease. It is possible that this is a temporary phenomenon, but it is cause for concern and an indication that dietary education to promote weight gain in a manner less likely to adversely affect the lipid profile is warranted.
Mary P. Miles, Sherri D. Pearson, Jan M. Andring, Jessy R. Kidd, and Stella L. Volpe
The purpose of this investigation was to determine whether carbohydrate supplementation during the frst 2 d post exercise recovery influenced the inflammation (IL-6, C-reactive protein [CRP], and cortisol) and muscle-damage responses. Eight participants performed a high-force eccentric elbow-fexion exercise to induce muscle soreness and inflammation and then consumed carbohydrate (0.25 g·kg−1·h−1) or an equal volume of placebo during hours 0–12 and 24–36 post exercise in a double-blind, crossover protocol. Muscle soreness; mid brachial arm circumference; blood glucose, IL-6, CRP, cortisol, and creatine-kinase (CK) activity; and maximal force production were measured pre exercise and 4, 8, 12, 24, 48, and 120 h post exercise. Plasma IL-6 increased, F(5) = 5.27, P < 0.05, 8 h post exercise, with no difference between carbohydrate and placebo conditions. Changes in muscle soreness, arm circumference, strength, and serum CK activity were consistent with small amounts of muscle damage and did not differ between conditions. The authors conclude that carbohydrate supplementation during recovery from soreness-inducing exercise does not influence the delayed IL-6 response temporally linked to inflammation or indications of muscle damage. Thus, increased carbohydrate consumption at levels consistent with recommendations for replenishing glycogen stores does not impair or promote the immune and muscle responses.
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.