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Biomedical subjects

M E Nevill

Publications and source records attributed to M E Nevill.

25 records · Page 2Linked to original sources

Effects of previous dynamic arm exercise on power output during repeated maximal sprint cycling.

This study examined the effects of elevating blood lactate concentration by arm exercise on subsequent performance during repeated 30 s sprints with the legs. Eight male students performed two 30 s cycle ergometer sprints separated by 6 min of recovery, on two occasions. On one occasion the subjects performed only the two 30 s cycle ergometer sprints ('legs'), while on the other occasion 5 min of heavy arm cranking preceded the two sprints ('arms and legs'). Blood lactate concentration was determined from capillary samples at rest, after a standardized warm-up and 3 and 5 min following each exercise bout. In the 'legs' condition, the peak power output (PPO) and mean power output (MPO) in the second sprint were 92% (P < 0.05) and 85% (P < 0.01) of the values attained during the first sprint, respectively. Prior arm exercise, which increased blood lactate to 11.0 +/- 0.6 mM, had no effect on PPO and MPO during the first cycle ergometer sprint (approximately 4% drop, N.S.). However, in the second sprint after prior arm exercise, PPO was 10% lower than the PPO attained during the corresponding sprint in the 'legs' condition (sprint 2 'arms and legs' 963 +/- 42 W, sprint 2 'legs' 1074 +/- 60 W, P < 0.05), while MPO was better maintained (sprint 2 'arms and legs' 517 +/- 17 W, sprint 2 'legs' 549 +/- 24 W, N.S.). The rate of blood lactate accumulation after both cycle ergometer sprints was considerably decreased (by approximately 50%) when blood lactate levels were pre-elevated by arm crank exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

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Accumulated oxygen deficit and short-distance running performance.

Recent studies have suggested that determining the accumulated oxygen deficit (AOD), in units of oxygen equivalents per kilogram body mass (ml O2 Eq.kg-1), during a short exhaustive run, may represent a non-invasive measure of anaerobic metabolism. However, there is little information either on the reproducibility of the laboratory determination or its relationship with human performance. The purpose of the present investigation was to determine the reproducibility of AOD during inclined treadmill running (study 1), and to examine its relationship with short-distance running performance (study 2). Twelve volunteers (11 males, 1 female) took part in study 1 and AOD was determined (relative exercise intensity approximately 120% VO2 max) on two separate occasions at a treadmill inclination of 10.5%; the laboratory-measured AOD values were 65.2 +/- 10.9 vs 66.3 +/- 12.5 ml O2 Eq.kg-1, respectively (r = 0.94, P < 0.01). A second subject group (10 males, 4 females) undertook study 2, which investigated AOD values and track times over 100, 400 and 800 m. The mean calculated AOD value was 66.1 +/- 12.0 ml O2 Eq.kg-1, and the average track times were 13.6 +/- 1.3, 60.9 +/- 6.8 and 138.8 +/- 18.5 s for the 100, 400 and 800 m, respectively. The r-values for the relationship between AOD and track time were -0.88, -0.82 (P < 0.01) and -0.61 (P < 0.05) for the 100, 400 and 800 m, respectively. The results of the present study suggest that the AOD (ml O2 Eq.kg-1) is a unique and reproducible physiological characteristic which is strongly correlated with sprint capacity.

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Effect of diet on performance during recovery from intermittent sprint exercise.

Eighteen games players (9 males, 9 females) performed 30 maximum 6-sprints on a non-motorized treadmill. Each sprint was preceded by a 60-s jog at 40% maximum speed and was followed by a 54-s walk at 20% maximum speed. Thus, the entire test was of 60-min duration. The subjects were then randomly assigned to three groups and repeated the 1-h test 24 h later after consuming either a high, normal or low carbohydrate diet (79 +/- 3, 47 +/- 8, 12 +/- 1% CHO, respectively). During trial 1, mean power output declined from 653 +/- 131 to 600 +/- 158 W during the 30 sprints (P < 0.01) and power output was lower during trial 2 than during trial 1 (n = 18, P < 0.01). During trial 2, there were no differences in sprint performance between the dietary groups for the exercise test as a whole (trial 2 mean power lower than trial 1 by 0.2, 0.5 and 5.0% for the high, normal and low CHO groups, respectively; N.S.), but if only the first nine sprints are considered, then the high CHO group performed better than the low CHO group (P < 0.05). Blood lactate and glucose concentrations were lower during trial 2 than trial 1 by 4.5, 13.8 and 29.0% (lactate) and 14.9, 11.3 and 35.8% (glucose) for the high, normal and low CHO groups, respectively (both P < 0.01). Thus, both the metabolic responses to, and the performance of, maximum intermittent exercise were reduced when the test was repeated after 24 h recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

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Repeated bouts of sprint running after induced alkalosis.

Seven healthy male subjects performed 10 maximal 6-s sprints, separated by 30-s recovery periods, on a non-motorized treadmill. On two occasions, separated by 3 days, the subjects ingested a solution of either sodium bicarbonate (NaHCO3; alkaline) or sodium chloride (NaCl; placebo), 2.5 h prior to exercise. The doses were 0.3 g kg-1 body mass for the alkaline treatment and 1.5 g total for the placebo, dissolved in 500 ml of water. The order of testing was randomly assigned. Pre-exercise blood pH was 7.43 +/- 0.02 and 7.38 +/- 0.01 for the alkaline and placebo trials respectively (P less than 0.01). Performance indices (i.e. mean and peak power outputs and mean and peak running speeds) were significantly reduced as a result of the cumulative effects of successive sprints, but not significantly affected by the treatments. However, the total work done (i.e. mean power output) in the alkaline condition was 2% higher than that achieved in the placebo condition. Post-exercise blood lactate concentrations were higher for the alkaline treatment than for the placebo condition (15.3 +/- 3.7 vs 13.6 +/- 3.0 mM respectively; P less than 0.01), but blood pH was similar in both conditions (alkaline: 7.15 +/- 0.13; placebo: 7.09 +/- 0.11). In both conditions, a relationship was found between post-exercise blood lactate and mean power output (alkaline: r = 0.82, P less than 0.01; placebo: r = 0.79, P less than 0.01). No significant differences were found in VE, VO2 and VCO2 between the two experimental conditions. This study demonstrates that alkali ingestion results in significant shifts in the acid-base balance of the blood, but has no effect on the power output during repeated bouts of brief maximal exercise.

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Physiological responses to maximal intermittent exercise: differences between endurance-trained runners and games players.

Six games players (GP) and six endurance-trained runners (ET) completed a standardized multiple sprint test on a non-motorized treadmill consisting of ten 6-s all-out sprints with 30-s recovery periods. Running speed, power output and oxygen uptake were determined during the test and blood samples were taken for the determination of blood lactate and pH. Games players tended to produce a higher peak power output (GP vs ET: 839 +/- 114 vs 777 +/- 89 W, N.S.) and higher peak speed (GP vs ET: 7.03 +/- 0.3 vs 6.71 +/- 0.3 m s-1, N.S.), but had a greater decrement in mean power output than endurance-trained runners (GP vs ET: 29.3 +/- 8.1% vs 14.2 +/- 11.1%, P less than 0.05). Blood lactate after the test was higher for the games players (GP vs ET: 15.2 +/- 1.9 vs 12.4 +/- 1.7 mM, P less than 0.05), but the decrease in pH was similar for both groups (GP vs ET: 0.31 +/- 0.08 vs 0.28 +/- 0.08, N.S.). Strong correlations were found between peak blood lactate and peak speed (r = 0.90, P less than 0.01) and between peak blood lactate and peak power fatigue (r = 0.92, P less than 0.01). The average increase in oxygen uptake above pre-exercise levels during the sprint test was greater for endurance-trained athletes than for the games players (ET vs GP: 35.0 +/- 2.2 vs 29.6 +/- 3.0 ml kg-1 min-1, P less than 0.05), corresponding to an average oxygen uptake per sprint (6-s sprint and 24 s of subsequent recovery) of 67.5 +/- 2.9% and 63.0 +/- 4.5% VO2 max respectively (N.S.). A modest relationship existed between the average increase in oxygen uptake above pre-exercise values during the sprint test and mean speed fatigue (r = -0.68, P less than 0.05). Thus, the greater decrement in performance for the games players may be related to higher glycolytic rates as reflected by higher lactate concentrations and to their lower oxygen uptake during the course of the 10 sprints.

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The hormonal responses to repetitive brief maximal exercise in humans.

The responses of nine men and nine women to brief repetitive maximal exercise have been studied. The exercise involved a 6-s sprint on a non-motorised treadmill repeated 10 times with 30 s recovery between each sprint. The total work done during the ten sprints was 37,693 +/- 3,956 J by the men and 26,555 +/- 4,589 J by the women (M greater than F, P less than 0.01). This difference in performance was not associated with higher blood lactate concentrations in the men (13.96 +/- 1.70 mmol.l-1) than the women (13.09 +/- 3.04 mmol.l-1). An 18-fold increase in plasma adrenaline (AD) occurred with the peak concentration observed after five sprints. The peak AD concentration in the men was larger than that seen in the women (9.2 +/- 7.3 and 3.7 +/- 2.4 nmol.l-1 respectively, P less than 0.05). The maximum noradrenaline (NA) concentration occurred after ten sprints in the men (31.6 +/- 10.9 nmol.l-1) and after five sprints in the women (27.4 +/- 20.8 nmol.l-1). Plasma cardiodilatin (CDN) and atrial natriuretic peptide (ANP) concentrations were elevated in response to the exercise. The peak ANP concentration occurred immediately post-exercise and the response of the women (10.8 +/- 4.5 pmol.l-1) was greater than that of the men (5.1 +/- 2.6 pmol.l-1, P less than 0.05). The peak CDN concentrations were 163 +/- 61 pmol.l-1 for the women and 135 +/- 61 pmol.l-1 for the men. No increases in calcitonin gene related peptide (CGRP) were detected in response to the exercise. These results indicate differences between men and women in performance and hormonal responses. There was no evidence for a role of CGRP in the control of the cardiovascular system after brief intermittent maximal exercise.

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Effect of training on muscle metabolism during treadmill sprinting.

Sixteen subjects volunteered for the study and were divided into a control (4 males and 4 females) and experimental group (4 males and 4 females, who undertook 8 wk of sprint training). All subjects completed a maximal 30-s sprint on a nonmotorized treadmill and a 2-min run on a motorized treadmill at a speed designed to elicit 110% of maximum oxygen uptake (110% run) before and after the period of training. Muscle biopsies were taken from vastus lateralis at rest and immediately after exercise. The metabolic responses to the 110% run were unchanged over the 8-wk period. However, sprint training resulted in a 12% (P less than 0.05) and 6% (NS) improvement in peak and mean power output, respectively, during the 30-s sprint test. This improvement in sprint performance was accompanied by an increase in the postexercise muscle lactate (86.0 +/- 26.4 vs. 103.6 +/- 24.6 mmol/kg dry wt, P less than 0.05) and plasma norepinephrine concentrations (10.4 +/- 5.4 vs. 12.1 +/- 5.3 nmol/l, P less than 0.05) and by a decrease in the postexercise blood pH (7.17 +/- 0.11 vs. 7.09 +/- 0.11, P less than 0.05). There was, however, no change in skeletal muscle buffering capacity as measured by the homogenate technique (67.6 +/- 6.5 vs. 71.2 +/- 4.5 Slykes, NS).

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