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Alannah K.A. McKay, Rachel McCormick, Nicolin Tee, and Peter Peeling

This study determined the impact of heat stress on postexercise inflammation and hepcidin levels. Twelve moderately trained males completed three, 60-min treadmill running sessions under different conditions: (a) COOL, 18 °C with speed maintained at 80% maximum heart rate; (b) HOTHR, 35 °C with speed maintained at 80% maximum heart rate; and (c) HOTPACE, 35 °C completed at the average running speed from the COOL trial. Venous blood samples were collected pre-, post-, and 3-hr postexercise and analyzed for serum ferritin, interleukin-6 (IL-6), and hepcidin concentrations. Average HR was highest during HOTPACE compared with HOTHR and COOL (p < .001). Running speed was slowest in HOTHR compared with COOL and HOTPACE (p < .001). The postexercise increase in IL-6 was greatest during HOTPACE (295%; p = .003). No differences in the IL-6 response immediately postexercise between COOL (115%) and HOTHR (116%) were evident (p = .992). No differences in hepcidin concentrations between the three trials were evident at 3 hr postexercise (p = .407). Findings from this study suggest the IL-6 response to exercise is greatest in hot compared with cool conditions when the absolute running speed was matched. No differences in IL-6 between hot and cool conditions were evident when HR was matched, suggesting the increased physiological strain induced from training at higher intensities in hot environments, rather than the heat per se, is likely responsible for this elevated response. Environmental temperature had no impact on hepcidin levels, indicating that exercising in hot conditions is unlikely to further impact transient alterations in iron regulation, beyond that expected in temperate conditions.

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Rebekah D. Alcock, Gregory C. Shaw, Nicolin Tee, Marijke Welvaert, and Louise M. Burke

The urinary excretion of hydroxyproline (Hyp), abundant in collagen protein, may serve as a biomarker of habitual collagen intake, assisting with investigations of current interest in the role of dietary collagen intake in supporting the synthesis of collagenous body tissues. This study investigated the time course of urinary Hyp excretion in “free-living,” healthy, active males following the ingestion of a standardized bolus (20 g) of collagenous (gelatin and a hydrolyzed collagen powder) and dairy (calcium caseinate and hydrolyzed casein) proteins. The excretion of Hyp was assessed over a 24-hr period, separated into three collection periods: 0–6, 6–12, and 12–24 hr. Hyp was elevated for 0–6 hr after the consumption of collagen-containing supplements (gelatin 31.3 ± 8.8 mmol/mol and hydrolyzed collagen 33.7 ± 22.0 mmol/mol vs. baseline: gelatin 2.4 ± 1.7 mmol/mol and hydrolyzed collagen 2.8 ± 1.5 mmol/mol; p < .05), but not for the dairy protein supplements (calcium caseinate 3.4 ± 1.7 mmol/mol and hydrolyzed casein 4.0 ± 3.7 mmol/mol; p > .05). Therefore, urinary Hyp reflects an acute intake of collagenous protein, but is not suitable as a biomarker for quantifying habitual collagen intake, provided through regular dietary practices in “free-living,” healthy, active males.

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Nikita C. Fensham, Alannah K.A. McKay, Nicolin Tee, Bronwen Lundy, Bryce Anderson, Aimee Morabito, Megan L.R. Ross, and Louise M. Burke

Previous research investigating single bouts of exercise have identified baseline iron status and circulating concentrations of interleukin-6 (IL-6) as contributors to the magnitude of postexercise hepcidin increase. The current study examined the effects of repeated training bouts in close succession on IL-6 and hepcidin responses. In a randomized, crossover design, 16 elite male rowers completed two trials, a week apart, with either high (1,000 mg) or low (<50 mg) calcium pre-exercise meals. Each trial involved two, submaximal 90-min rowing ergometer sessions, 2.5 hr apart, with venous blood sampled at baseline; pre-exercise; and 0, 1, 2, and 3 hr after each session. Peak elevations in IL-6 (approximately 7.5-fold, p < .0001) and hepcidin (approximately threefold, p < .0001) concentrations relative to baseline were seen at 2 and 3 hr after the first session, respectively. Following the second session, concentrations of both IL-6 and hepcidin remained elevated above baseline, exhibiting a plateau rather than an additive increase (2 hr post first session vs. 2 hr post second session, p = 1.00). Pre-exercise calcium resulted in a slightly greater elevation in hepcidin across all time points compared with control (p = .0005); however, no effect on IL-6 was evident (p = .27). Performing multiple submaximal training sessions in close succession with adequate nutritional support does not result in an amplified increase in IL-6 or hepcidin concentrations following the second session in male elite rowers. Although effects of calcium intake require further investigation, athletes should continue to prioritize iron consumption around morning exercise prior to exercise-induced hepcidin elevations to maximize absorption.

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Alannah K.A. McKay, Peter Peeling, David B. Pyne, Nicolin Tee, Marijke Welveart, Ida A. Heikura, Avish P. Sharma, Jamie Whitfield, Megan L. Ross, Rachel P.L. van Swelm, Coby M. Laarakkers, and Louise M. Burke

This study implemented a 2-week high carbohydrate (CHO) diet intended to maximize CHO oxidation rates and examined the iron-regulatory response to a 26-km race walking effort. Twenty international-level, male race walkers were assigned to either a novel high CHO diet (MAX = 10 g/kg body mass CHO daily) inclusive of gut-training strategies, or a moderate CHO control diet (CON = 6 g/kg body mass CHO daily) for a 2-week training period. The athletes completed a 26-km race walking test protocol before and after the dietary intervention. Venous blood samples were collected pre-, post-, and 3 hr postexercise and measured for serum ferritin, interleukin-6, and hepcidin-25 concentrations. Similar decreases in serum ferritin (17–23%) occurred postintervention in MAX and CON. At the baseline, CON had a greater postexercise increase in interleukin-6 levels after 26 km of walking (20.1-fold, 95% CI [9.2, 35.7]) compared with MAX (10.2-fold, 95% CI [3.7, 18.7]). A similar finding was evident for hepcidin levels 3 hr postexercise (CON = 10.8-fold, 95% CI [4.8, 21.2]; MAX = 8.8-fold, 95% CI [3.9, 16.4]). Postintervention, there were no substantial differences in the interleukin-6 response (CON = 13.6-fold, 95% CI [9.2, 20.5]; MAX = 11.2-fold, 95% CI [6.5, 21.3]) or hepcidin levels (CON = 7.1-fold, 95% CI [2.1, 15.4]; MAX = 6.3-fold, 95% CI [1.8, 14.6]) between the dietary groups. Higher resting serum ferritin (p = .004) and hotter trial ambient temperatures (p = .014) were associated with greater hepcidin levels 3 hr postexercise. Very high CHO diets employed by endurance athletes to increase CHO oxidation have little impact on iron regulation in elite athletes. It appears that variations in serum ferritin concentration and ambient temperature, rather than dietary CHO, are associated with increased hepcidin concentrations 3 hr postexercise.