Title

The Acute Effects of Nutrition on Muscle Signaling and Hormonal Responses to Consecutive Repeated Sprints and Resistance Exercise

Date of Completion

January 2010

Keywords

Biology, Molecular|Health Sciences, Nutrition|Health Sciences, Recreation

Degree

Ph.D.

Abstract

Exercise provides a potent stimulus for skeletal muscle remodeling. The modality and intensity of a given exercise protocol can initiate molecular signaling and hormonal cascades that induce phenotypic adaptations specific to the training stimulus. Therefore, the purpose of this study was to examine the effect of a nutritional supplement on the anabolic and catabolic signaling and hormonal responses to consecutive divergent exercise bouts. Eight healthy, highly-trained men (mean ± SE age: 27.4 ± 1.92 y; height: 180.4 ± 2.4 cm; wt: 92.7 ± 3.9 kg; body fat 15.8 ± 1.9%) completed two trials that consisted of a bout of resistance exercise (RE) (5 sets of 5 reps of front squat at 80% 1RM) followed 15 minutes later by repeated sprints (RS) (8x 10s maximal running sprints with 45s rest). In this randomized cross-over design, subjects consumed a protein plus carbohydrate (P+C) nutritional supplement between the RE and RS during one trial, and consumed the equivalent volume of water during the other trial. Trials were separated by one week. p70 S6k Total values were 31% greater for the supplement versus non-supplement group (p<0.05). There were no significant differences between trials for Akt Total or 4E-BP1. Cortisol values peaked at +30 (1171.45 ± 17.1 nmol/L) and were significantly higher than baseline at this time point (p<0.05). Mean testosterone values were significantly greater than baseline at all time points (p<0.05), (mean PRE1 values 26.53 ± 0.48 nmol/L), while the mean testosterone to cortisol ratio (T:C) was 1:31, possibly indicating an altered anabolic to catabolic state. Contrary to our hypothesis, nutritional intervention did not appear to facilitate phosphorylation of p70 S6k at the Thr389 activation site. It is possible the high cortisol values present and/or the elevated training status of our subject population contributed to the lack of signaling response for p70 S6k at Thr389. ^