The current case study attempted to document the contemporary demands of elite rugby union. Players (n = 2) were tracked continuously during a competitive team selection game using Global Positioning System (GPS) software. Data revealed that players covered on average 6,953 m during play (83 minutes). Of this distance, 37% (2,800 m) was spent standing and walking, 27% (1,900 m) jogging, 10% (700 m) cruising, 14% (990 m) striding, 5% (320 m) high-intensity running, and 6% (420 m) sprinting. Greater running distances were observed for both players (6.7% back; 10% forward) in the second half of the game. Positional data revealed that the back performed a greater number of sprints (>20 km x h(-1)) than the forward (34 vs. 19) during the game. Conversely, the forward entered the lower speed zone (6-12 km x h(-1)) on a greater number of occasions than the back (315 vs. 229) but spent less time standing and walking (66.5 vs. 77.8%). Players were found to perform 87 moderate-intensity runs (>14 km x h(-1)) covering an average distance of 19.7 m (SD = 14.6). Average distances of 15.3 m (back) and 17.3 m (forward) were recorded for each sprint burst (>20 km x h(-1)), respectively. Players exercised at approximately 80 to 85% VO2max during the course of the game with a mean heart rate of 172 b x min(-1) ( approximately 88% HRmax). This corresponded to an estimated energy expenditure of 6.9 and 8.2 MJ, back and forward, respectively. The current study provides insight into the intense and physical nature of elite rugby using "on the field" assessment of physical exertion. Future use of this technology may help practitioners in design and implementation of individual position-specific training programs with appropriate management of player exercise load.

ObjectivesNational dietary guidelines were introduced in 1977 and 1983, by the US and UK governments, respectively, with the ambition of reducing coronary heart disease (CHD) by reducing fat intake. To date, no analysis of the evidence base for these recommendations has been undertaken. The present study examines the evidence from randomised controlled trials (RCTs) available to the US and UK regulatory committees at their respective points of implementation.MethodsA systematic review and meta-analysis were undertaken of RCTs, published prior to 1983, which examined the relationship between dietary fat, serum cholesterol and the development of CHD.Results2467 males participated in six dietary trials: five secondary prevention studies and one including healthy participants. There were 370 deaths from all-cause mortality in the intervention and control groups. The risk ratio (RR) from meta-analysis was 0.996 (95% CI 0.865 to 1.147). There were 207 and 216 deaths from CHD in the intervention and control groups, respectively. The RR was 0.989 (95% CI 0.784 to 1.247). There were no differences in all-cause mortality and non-significant differences in CHD mortality, resulting from the dietary interventions. The reductions in mean serum cholesterol levels were significantly higher in the intervention groups; this did not result in significant differences in CHD or all-cause mortality. Government dietary fat recommendations were untested in any trial prior to being introduced.ConclusionsDietary recommendations were introduced for 220 million US and 56 million UK citizens by 1983, in the absence of supporting evidence from RCTs.

SummaryAcclimatisation to environmental hypoxia initiates a series of metabolic and musculocardiorespiratory adaptations that influence oxygen transport and utilisation. Whilst it is clear that adequate acclimatisation, or better still, being born and raised at altitude, is necessary to achieve optimal physical performance at altitude, scientific evidence to support the potentiating effects after return to sea level is at present equivocal. Despite this, elite athletes continue to spend considerable time and resources training at altitude, misled by subjective coaching opinion and the inconclusive findings of a large number of uncontrolled studies. Scientific investigation has focused on the optimisation of the theoretically beneficial aspects of altitude acclimatisation, which include increases in blood haemoglobin concentration, elevated buffering capacity, and improvements in the structural and biochemical properties of skeletal muscle. However, not all aspects of altitude acclimatisation are beneficial; cardiac output and blood flow to skeletal muscles decrease, and preliminary evidence has shown that hypoxia in itself is responsible for a depression of immune function and increased tissue damage mediated by oxidative stress. Future research needs to focus on these less beneficial aspects of altitude training, the implications of which pose a threat to both the fitness and the health of the elite competitor.Paul Bert was the first investigator to show that acclimatisation to a chronically reduced inspiratory partial pressure of oxygen (PIo,) invoked a series of central and peripheral adaptations that served to maintain adequate tissue oxygenation in healthy skeletal muscle,' physiological adaptations that have been subsequently implicated in the improvement in exercise performance during altitude acclimatisation. However, it was not until half a century later that scientists suggested that the additive stimulus of environmental hypoxia could potentially compound the normal physiological adaptations to endurance training and accelerate performance improvements after return to sea level. This has stimulated an exponential increase in scientific research, and, since 1984, 22 major reviews have summarised the physiological implications of altitude training for both aerobic and anaerobic performance at altitude and after return to sea level. Of these reviews, only eight have specifically focused on physical performance changes after return to sea level,2-9 the most comprehensive of which was recently written by Wolski et al. 9 Few reviews have considered the potentially less favourable physiological responses to moderate altitude exposure, which include decreases in absolute training intensity,'0 decreased plasma volume," depression of haemopoiesis and increased haemolysis,12 increases in sympathetically mediated glycogen depletion at altitude,'3 and increased respiratory muscle work after return to sea level.'4 In addition, there is a risk of developing more serious medical complications at altitude, which inclu...

Elite distance runners participated in one of two studies designed to investigate the e ects of moderate altitude training (inspiratory partial pressure of oxygen »115±125 mmHg) on submaximal, maximal and supramaximal exercise performance following return to sea-level. Study 1 (New Mexico, USA) involved 14 subjects who were assigned to a 4-week altitude training camp (1500±2000 m) whilst 9 performance-matched subjects continued with an identical training programme at sea-level (CON). Ten EXP subjects who trained at 1640 m and 19 CON subjects also participated in study 2 (Krugersdorp, South Africa). Selected metabolic and cardiorespiratory parameters were determined with the subjects at rest and during exercise 21 days prior to (PRE) and 10 and 20 days following their return to sealevel (POST). Whole blood lactate decreased by 23% (P < 0.05 vs PRE) during submaximal exercise in the EXP group only after 20 days at sea-level (study 1). However, the lactate threshold and other measures of running economy remained unchanged. Similarly, supramaximal performance during a standardised track session did not change. Study 2 demonstrated that hypoxia per se did not alter performance. In contrast, in the EXP group supramaximal running velocity decreased by 2% (P < 0.05) after 20 days at sea-level.Both studies were characterised by a 50% increase in the frequency of upper respiratory and gastrointestinal tract infections during the altitude sojourns, and two male subjects were diagnosed with infectious mononucleosis following their return to sea-level (study 1). Group mean plasma glutamine concentrations at rest decreased by 19% or 143 (74) lM (P < 0.001) after 3 weeks at altitude, which may have been implicated in the increased incidence of infectious illness.

ObjectivesNational dietary guidelines were introduced in 1977 and 1983, by the USA and UK governments, respectively, with the ambition of reducing coronary heart disease (CHD) mortality by reducing dietary fat intake. A recent systematic review and meta-analysis by the present authors, examining the randomised controlled trial (RCT) evidence available to the dietary committees during those time periods, found no support for the recommendations to restrict dietary fat. The present investigation extends our work by re-examining the totality of RCT evidence relating to the current dietary fat guidelines.MethodsA systematic review and meta-analysis of RCTs currently available, which examined the relationship between dietary fat, serum cholesterol and the development of CHD, was undertaken.ResultsThe systematic review included 62 421 participants in 10 dietary trials: 7 secondary prevention studies, 1 primary prevention and 2 combined. The death rates for all-cause mortality were 6.45% and 6.06% in the intervention and control groups, respectively. The risk ratio (RR) from meta-analysis was 0.991 (95% CI 0.935 to 1.051). The death rates for CHD mortality were 2.16% and 1.80% in the intervention and control groups, respectively. The RR was 0.976 (95% CI 0.878 to 1.084). Mean serum cholesterol levels decreased in all intervention groups and all but one control group. The reductions in mean serum cholesterol levels were significantly greater in the intervention groups; this did not result in significant differences in CHD or all-cause mortality.ConclusionsThe current available evidence found no significant difference in all-cause mortality or CHD mortality, resulting from the dietary fat interventions. RCT evidence currently available does not support the current dietary fat guidelines. The evidence per se lacks generalisability for population-wide guidelines.