Philip R. Hayes, Kjell van Paridon, Duncan N. French, Kevin Thomas and Dan A. Gordon
The aim of this study was to develop a laboratory-based treadmill simulation of the on-course physiological demands of an 18-hole round of golf and to identify the underlying physiological responses.
Eight amateur golfers completed a round of golf during which heart rate (HR), steps taken, and global positioning system (GPS) data were assessed. The GPS data were used to create a simulated discontinuous round on a treadmill. Steps taken and HR were recorded during the simulated round.
During the on-course round, players covered a mean (±SD) of 8,251 ± 450 m, taking 12,766 ± 1,530 steps. The mean exercise intensity during the on-course round was 31.4 ± 9.3% of age-predicted heart rate reserve (%HRR) or 55.6 ± 4.4% of age-predicted maximum HR (%HRmax). There were no significant differences between the simulated round and the on-course round for %HRR (P = .537) or %HR max (P = .561) over the entire round or for each individual hole. Furthermore, there were no significant differences between the two rounds for steps taken. Typical error values for steps taken, HR, %HRmax, and %HRR were 1,083 steps, ±7.6 b·min-1, ±4.5%, and ±8.1%, respectively.
Overall, the simulated round of golf successfully recreated the demands of an on-course round. This simulated round could be used as a research tool to assess the extent of fatigue during a round of golf or the impact of various interventions on golfers.
Thomas I. Gee, Duncan N. French, Karl C. Gibbon and Kevin G. Thompson
This study investigated the pacing strategy adopted and the consistency of performance and related physiological parameters across three 2000-m rowing-ergometer tests.
Fourteen male well-trained rowers took part in the study. Each participant performed three 2000-m rowing-ergometer tests interspersed by 3–7 d. Throughout the trials, respiratory exchange and heart rate were recorded and power output and stroke rate were analyzed over each 500 m of the test. At the completion of the trial, assessments of blood lactate and rating of perceived exertion were measured.
Ergometer performance was unchanged across the 3 trials; however, pacing strategy changed from trial 1, which featured a higher starting power output and more progressive decrease in power, to trials 2 and 3, which were characterized by a more conservative start and an end spurt with increased power output during the final 500 m. Mean typical error (TE; %) across the three 2000-m trials was 2.4%, and variability was low to moderate for all assessed physiological variables (TE range = 1.4−5.1%) with the exception of peak lactate (TE = 11.5%).
Performance and physiological responses during 2000-m rowing ergometry were found to be consistent over 3 trials. The variations observed in pacing strategy between trial 1 and trials 2 and 3 suggest that a habituation trial is required before an intervention study and that participants move from a positive to a reverse-J-shaped strategy, which may partly explain conflicting reports in the pacing strategy exhibited during 2000-m rowing-ergometer trials.
Thomas W. Jones, Ian H. Walshe, David L. Hamilton, Glyn Howatson, Mark Russell, Oliver J. Price, Alan St Clair Gibson and Duncan N. French
To compare anabolic signaling responses to differing sequences of concurrent strength and endurance training in a fed state.
Eighteen resistance-trained men were randomly assigned to the following experimental conditions: strength training (ST), strength followed by endurance training (ST-END), or endurance followed by strength training (END-ST). Muscle tissue samples were taken from the vastus lateralis before each exercise protocol, on cessation of exercise, and 1 h after cessation of strength training. Tissue was analyzed for total and phosphorylated (p-) signaling proteins linked to the mTOR and AMPK networks.
Strength-training performance was similar between ST, ST-END, and END-ST. p-S6k1 was elevated from baseline 1 h posttraining in ST and ST-END (both P < .05). p-4E-BP1 was significantly lower than baseline post-ST (P = .01), whereas at 1 h postexercise in the ST-END condition p-4E-BP1 was significantly greater than postexercise (P = .04). p-ACC was elevated from baseline both postexercise and 1 h postexercise (both P < .05) in the END-ST condition. AMPK, mTOR, p38, PKB, and eEF2 responded similarly to ST, ST-END, and END-ST. Signaling responses to ST, ST-END, and END were largely similar. As such it cannot be ascertained which sequence of concurrent strength and endurance training is most favorable in promoting anabolic signaling.
In the case of the current study an acute bout of concurrent training of differing sequences elicited similar responses of the AMPK and mTOR networks.
William J. Kraemer, Ana L. Gómez, Nicholas A. Ratamess, Jay R. Hoffman, Jeff S. Volek, Martyn R. Rubin, Timothy P. Scheett, Michael R. McGuigan, Duncan French, Jaci L. VanHeest, Robbin B. Wickham, Brandon Doan, Scott A. Mazzetti, Robert U. Newton and Carl M. Maresh
To determine the effects of Vicoprofen®, ibuprofen, and placebo on anaerobic performance and pain relief after resistance-exercise-induced muscle damage.
Randomized, controlled clinical study.
University human-performance/sports-medicine laboratory.
36 healthy men.
Methods and Measures:
After baseline testing (72 h), participants performed an eccentric-exercise protocol. Each was evaluated for pain 24 h later and randomly assigned to a Vicoprofen (VIC), ibuprofen (IBU), or placebo (P) group. Postexercise testing was performed every 24 h for 4 d.
Significantly greater muscle force, power, and total work were observed in VIC than in P (P < .05) for most time points and for IBU at 48 h.
Anaerobic performance is enhanced with VIC, especially within the first 24 h after significant muscle-tissue damage. The greater performances observed at 48 h might be a result of less damage at this time point with VIC treatment.