This paper provides a thumb-nail sketch of some of the key issues that have been instrumental in the development of the scientific study of exercise, and more particularly sports, physiology. Those who have had the pleasure of reading the American Physiological Society's publication Exercise Physiology in its "People and Ideas" series, will know the breadth and depth of the extant material in this field. In an attempt at some form of coherence, the present paper focuses on the concepts of maximal oxygen uptake and oxygen debt introduced by the British physiologist Archibald Vivian Hill in 1922. The Introduction provides a contextual framework for the paper, and is followed by a description of the work undertaken by Hill and his colleagues in the development of these concepts over a three-year period. Credit is given to scientists from the eighteenth century onwards who provided the scientific foundations that led to the measurement of oxygen uptake, and those who went on to elaborate the physiological mechanisms of aerobic and anaerobic metabolism. The problems in what constitutes a plateau and how to get it are discussed, along with attempts to predict maximal oxygen uptake from sub-maximal--or even no--exercise. The debate surrounding the limiting factor in the oxygen uptake chain started by Hill is brought up to date rather than resolved. The ecological validity of applied sports physiology is explored in terms of sport-specific ergometry and test protocols. Finally, Hill's interest in the production and removal of lactic acid re-emerges in the recent attempts to establish the threshold at which accumulation of lactic acid in the blood leads to cessation of exercise, and also the means of validly measuring an individual's anaerobic power and capacity. Wherever possible and appropriate, counter-arguments are introduced to demonstrate the transient and uncertain nature of what is often regarded as true knowledge.

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In this study, we tested the hypothesis that elite dinghy sailing is a whole-body, dynamic, repeated-effort sport, and that increased heart rate and oxygen consumption reflect its dynamic element. Six elite male Laser sailors (mean age 19.7 years, s = 1.82; height 1.81 m, s = 0.03; body mass 78.0 kg, s = 4.1) performed a cycle ergometer test to volitional exhaustion to determine peak oxygen uptake (VO(2peak)) and a simulated 30-min upwind leg sail on a specially constructed Laser sailing ergometer. The simulation protocol was based on video analysis of previous Laser World Championships. Expired gases were collected in Douglas bags, heart rate recorded at rest and after every 5 min, and pre- and post-simulation capillary blood samples taken for blood lactate analysis. Results were analysed with a one-way analysis of variance. Mean VO(2peak) was 4.32 l . min(-1) (s = 0.16). Mean simulation VO(2) was 2.51 l . min(-1) (s = 0.24) and peaked at 2.58 l . min(-1) (s = 0.25) during the 5th minute. Mean simulation heart rate was 156 beats . min(-1) (s = 8), peaking during the final minute at 160 beats . min(-1) (s = 10). These results suggest that, unlike pseudo-isometric static hiking, elite dinghy sailing demands a substantial proportion (58%VO(2peak), s = 5.6) of aerobic capacity.

The physiological effects of strategies for a rapid loss of body mass immediately before weighing-in for competition in weight-governed sports are unclear. This study examined the effects of a 3%-4% loss in body mass on a boxing-related task. Seven novice amateur boxers completed three 3 min rounds of simulated boxing on a prototype boxing ergometer in an euhydrated state (E-trial) and after exercise-induced thermal dehydration (D-trial). All subjects lost body mass following dehydration-mean body mass fell 3.8 (SD +/- 0.3)% [77.3 (SD +/- 11.3) to 74.4 (SD +/- 10.7) kg, P<0.001] - but changes in plasma volume (PV) were inconsistent. Four subjects suffered reductions in PV between 15% and 30%, one subject maintained his E-trial value and two recorded an increase. The D-trial mean PV value was 8.0 (SD +/- 17.2)% lower but this fall was not statistically significant (P>0.05). Analysis of D-trial boxing performance showed one subject maintained his performance over the two trials and a second improved 17.8%. A two-way ANOVA (condition x time) with repeated measures on both factors showed no significant main effect differences for condition (F1,6 = 3.93 P>0.05), time (F1.83,48 = 1.12, P>0.05) or interaction between them (F1.93,48, P>0.05). Furthermore, neither heart rate nor blood lactate responses in the boxing task differed between trials. These data were affected by the small sample. Power and effect size analysis using eta(2) procedure and removing the outlier data produced a mean fall in boxing performance of 26.8%. However, some subjects appeared able to resist the deleterious effects of a rapid loss of body mass prior to competition and further research is needed to explain the mechanisms under-pinning this ability.

This study examined the effects of serial reductions in energy and fluid intake on two simulated boxing performances separated by 2 days recovery. Eight amateur boxers (age: 23.6 +/- 3.2 years; height 175 +/- 5 cm; body mass [BM] 73.3 +/- 8.3 kg [Mean +/- SD]) performed two simulated boxing bouts (BB) under normal (N-trial) and restricted (R-trial) diets in a counterbalanced design over 5 days. The trials were separated by a 9-day period of normal dietary behavior (X-trial). BM was recorded on days 1, 3, and 5 of each trial. Simulated bouts of three, 3-min rounds with 1-min recovery were completed on days 3 (BB1) and 5 (BB2) of each 5-day trial. Punching force (N) was recorded from 8 sets of 7 punches by a purpose-built boxing ergometer. Heart rate (fC) was monitored continuously (PE3000 Polar Sports Tester, Kempele, Finland), and blood lactate (BLa) and glucose (BG) were determined 4-min post-performance (2300 StaPlus, YSI, Ohio). Energy and fluid intakes were significantly lower in the R-trial (p < .05). Body mass was maintained during the N-trial but fell 3% (p < .05) during the R-trial. There were no significant differences in end-of-bout fC or post-bout BG, but BLa was higher in the N- than the R-trial (p < .05). R-trial punching forces were 3.2% and 4.6% lower, respectively, compared to the corresponding N-trial bouts, but the differences did not reach statistical significance. These results suggest that energy and fluid restrictions in weight-governed sports do not always lead to a significant decrease in performance, but because of the small sample size and big variations in individual performances, these findings should be interpreted with care.

Introduction: This study examined the effect of massage on delayed onset muscle soreness of quadriceps muscles and single leg vertical jump performance after downhill treadmill walking. Methods: Seven moderately active females (age: 19 ± 1 yr, height: 168 ± 3 cm, body mass: 63.9 ± 5.5 kg) completed a 20 min downhill walk (speed: 6.4 km•h-1 , gradient:-25%) as they carried a load equal to 10% of their body mass followed by one leg receiving massage for 25 min. Before, 24, 48 and 72 hr after downhill walking, delayed onset muscle soreness on a scale of 1-10 from rectus femoris (RF), vastus medialis (VM) and vastus lateralis (VL) muscles and changes in single leg vertical jump performance were measured for both legs. Results: Delayed onset muscle soreness was reduced by massage 48 hr post-exercise in the RF and VL (P<0.05) but not in the VM. Jumping performance of each leg declined after downhill walking (P<0.001). At 24 hours, jumping height was decreased by 19% and 21% in control and massaged leg, respectively (P<0.05). However, at 48 and 72 hr post-exercise, the massaged leg showed improved recovery in jumping performance. Conclusions: Reductions in delayed onset muscle soreness of quadriceps muscles by massage after downhill walking were muscle-specific. Massage improved functional recovery after downhill walking.

Results reveal postural sway deficits in ankles with FAI. They also demonstrate a significant relationship between PL and PB reaction times and postural sway in UA. Individuals who sustain an acute ankle sprain and those with FAI require rehabilitation that improves proprioception, strengthens the evertors and dorsiflexors, and restores peroneal reaction time.

Results demonstrate a deficit (slower reaction time) in ankles with FAI when acting in support and when exposed to a simulated sprain compared to stable healthy controls. As a result of slower reaction times, acting to support the UA may put the contralateral SA at an increased risk of ankle sprain. This suggests that rehabilitation of a lateral ankle sprain should include strengthening the evertors (peroneals and EDL) at the subtalar joint and the dorsiflexors (TA and EDL) at the talocrural joint.