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Biomedical subjects

G S Palmer

Publications and source records attributed to G S Palmer.

At least 19 recordsLinked to original sources

The ecological validity of laboratory cycling: Does body size explain the difference between laboratory- and field-based cycling performance?

Previous researchers have identified significant differences between laboratory and road cycling performances. To establish the ecological validity of laboratory time-trial cycling performances, the causes of such differences should be understood. Hence, the purpose of the present study was to quantify differences between laboratory- and road-based time-trial cycling and to establish to what extent body size [mass (m) and height (h)] may help to explain such differences. Twenty-three male competitive, but non-elite, cyclists completed two 25 mile time-trials, one in the laboratory using an air-braked ergometer (Kingcycle) and the other outdoors on a local road course over relatively flat terrain. Although laboratory speed was a reasonably strong predictor of road speed (R2 = 69.3%), a significant 4% difference (P < 0.001) in cycling speed was identified (laboratory vs. road speed: 40.4 +/- 3.02 vs. 38.7 +/- 3.55 km x h(-1); mean +/- s). When linear regression was used to predict these differences (Diff) in cycling speeds, the following equation was obtained: Diff (km x h(-1)) = 24.9 - 0.0969 x m - 10.7 x h, R2 = 52.1% and the standard deviation of residuals about the fitted regression line = 1.428 (km . h-1). The difference between road and laboratory cycling speeds (km x h(-1)) was found to be minimal for small individuals (mass = 65 kg and height = 1.738 m) but larger riders would appear to benefit from the fixed resistance in the laboratory compared with the progressively increasing drag due to increased body size that would be experienced in the field. This difference was found to be proportional to the cyclists' body surface area that we speculate might be associated with the cyclists' frontal surface area.

Adult↗

Scaling maximal oxygen uptake to predict cycling time-trial performance in the field: a non-linear approach.

The purpose of the present article is to identify the most appropriate method of scaling VO2max for differences in body mass when assessing the energy cost of time-trial cycling. The data from three time-trial cycling studies were analysed (N = 79) using a proportional power-function ANCOVA model. The maximum oxygen uptake-to-mass ratio found to predict cycling speed was VO2max(m)(-0.32) precisely the same as that derived by Swain for sub-maximal cycling speeds (10, 15 and 20 mph). The analysis was also able to confirm a proportional curvilinear association between cycling speed and energy cost, given by (VO2max(m)(-0.32))0.41. The model predicts, for example, that for a male cyclist (72 kg) to increase his average speed from 30 km h(-1) to 35 km h(-1), he would require an increase in VO2max from 2.36 l min(-1) to 3.44 l min(-1), an increase of 1.08 l min(-1). In contrast, for the cyclist to increase his mean speed from 40 km h(-1) to 45 km h(-1), he would require a greater increase in VO2max from 4.77 l min(-1) to 6.36 l min(-1), i.e. an increase of 1.59 l min(-1). The model is also able to accommodate other determinants of time-trial cycling, e.g. the benefit of cycling with a side wind (5% faster) compared with facing a predominately head/tail wind (P<0.05). Future research could explore whether the same scaling approach could be applied to, for example, alternative measures of recording power output to improve the prediction of time-trial cycling performance.

Adult↗

Comparison of physiological responses to open water kayaking and kayak ergometry.

This study compared the physiological responses of simulated kayaking on a K1 ERGO kayak ergometer with open water paddling. Nine well-trained male kayakers (VO2peak 4.27 +/- 0.58 L x min(-1), age 24 +/- 4 yr, mass 77.3 +/- 6.4 kg, height 179.5 +/- 5.3 cm; [mean +/- SD]) performed two 4 min exercise bouts on open water (OW) and on an air braked kayak ergometer (Erg). During exercise, expired air and heart rate (HR) were continuously measured. The distance covered during OW (992 +/- 47.1 m) was highly correlated (r2 = 0.86) with the total work performed in Erg (47.64 +/- 7.67 kJ). There were no differences between trials for oxygen uptake, carbon dioxide production or estimated carbohydrate oxidation. However, during OW, minute ventilation was significantly higher at 60 and 90 s (104.2 +/- 16.4 vs. 92.6 +/- 20.4 L x min(-1) and 120.5 +/- 15.8 vs. 111.7 +/- 17.6 L x min(-1) for 60 and 90 s, respectively, p < 0.05), and HR was higher in OW during the first minute (120 +/- 20 vs. 104 +/- 19 beats x min(-1), 164 +/- 8 vs. 147 +/- 18 beats x min(-1) and 178 +/- 6 vs. 170 +/- 7 beats x min(-1) for 0, 30, and 60 s, respectively, p < 0.05). There were no differences in peak VO2 between OW and Erg (4.10 +/- 0.49 vs. 4.09 +/- 0.53 L x min(-1), respectively) nor in post-exercise blood (lactate) (6.43 +/- 1.47 vs. 6.59 +/- 0.99 mmol x L(-1), respectively). We conclude that the K1 ERGO accurately simulates the physiological demands of short-term, high-intensity kayaking.

Adolescent↗

Metabolic and performance responses to constant-load vs. variable-intensity exercise in trained cyclists.

We studied glucose oxidation (Glu(ox)) and glycogen degradation during 140 min of constant-load [steady-state (SS)] and variable-intensity (VI) cycling of the same average power output, immediately followed by a 20-km performance ride [time trial (TT)]. Six trained cyclists each performed four trials: two experimental bouts (SS and VI) in which muscle biopsies were taken before and after 140 min of exercise for determination of glycogen and periodic acid-Schiff's staining; and two similar trials without biopsies but incorporating the TT. During two of the experimental rides, subjects ingested a 5 g/100 ml [U-(14)C]glucose solution to determine rates of Glu(ox). Values were similar between SS and VI trials: O(2) consumption (3.08 +/- 0.02 vs. 3.15 +/- 0.03 l/min), energy expenditure (901 +/- 40 vs. 904 +/- 58 J x kg(-1) x min(-1)), heart rate (156 +/- 1 vs. 160 +/- 1 beats/min), and rating of perceived exertion (12.6 +/- 0.6 vs. 12.7 +/- 0.7). However, the area under the curve for plasma lactate concentration vs. time was significantly greater during VI than SS (29.1 +/- 3.9 vs. 24.6 +/- 3. 7 mM/140 min; P = 0.03). VI resulted in a 49% reduction in total muscle glycogen utilization vs. 65% for SS, while total Glu(ox) was higher (99.2 +/- 5.3 vs. 83.9 +/- 5.2 g/140 min; P < 0.05). The number of glycogen-depleted type I muscle fibers at the end of 140 min was 98% after SS but only 59% after VI. Conversely, the number of type II fibers that showed reduced periodic acid-Schiff's staining was 1% after SS vs. 10% after VI. Despite these metabolic differences, subsequent TT performance was similar (29.14 +/- 0.9 vs. 30.5 +/- 0.9 min for SS vs. VI). These results indicate that whole body metabolic and cardiovascular responses to 140 min of either SS or VI exercise at the same average intensity are similar, despite differences in skeletal muscle carbohydrate metabolism and recruitment.

Adolescent↗

Carbohydrate ingestion immediately before exercise does not improve 20 km time trial performance in well trained cyclists.

This study examined the effects of carbohydrate ingestion on 20 km cycle time-trial (TT) performance in 14 well-trained cyclists (11 males, 3 females; peak oxygen uptake [VO2peak] 4.52 +/- 0.60 l/min; values are mean +/- SD). All subjects performed two experimental trials on their own bicycles mounted on an air-braked ergometry system (Kingcycle). Subjects were instructed to maintain the same training and dietary regimens before trials, which were conducted in a random order, 3-7 days apart, and at the same time of day for each subject. On the day of a trial, subjects reported to the laboratory and ingested an 8 ml/kg body mass bolus of either a 6.8 g/100 ml commercial carbohydrate-electrolyte (CHO) beverage (39 +/- 4 g of CHO), or a coloured, flavoured placebo. Ten min after finishing the drink, subjects commenced a 5 min warm-up at 150 W, before commencing the 20 km TT. The average power output (312 +/- 40 vs 311 +/- 38 W) and heart-rate (171 +/- 6 vs 171 +/- 5 beats/min for CHO and placebo, respectively) during the two rides did not differ between treatments. Accordingly, the performance times for the two TT's were the same (27:41 +/- 1:39 min:sec, for both CHO and placebo). We conclude that the ingestion of approximately 40 g of carbohydrate does not improve maximal cycling performance lasting approximately 30 min, and that carbohydrate availability, in the form of circulating blood glucose, does not limit high-intensity exercise of this duration.

Adolescent↗

Effects of 3 days of carbohydrate supplementation on muscle glycogen content and utilisation during a 1-h cycling performance.

This study compared the effects of supplementing the normal diets of six trained cyclists [maximal oxygen uptake (VO2max) 4.5 (0.36) l.min-1; values are mean (SD)] with additional carbohydrate (CHO) on muscle glycogen utilisation during a 1-h cycle time-trial (TT). Using a randomised crossover design, subjects consumed either their normal diet (NORM) for 3 days, which consisted of 426 (137) g.day-1 CHO [5.9 (1.4) g. kg-1 body mass (BM)], or additional CHO (SUPP) to increase their intake to 661 (76) g.day-1 [9.3 (0.7) g. kg-1 BM]. The SUPP diet elevated muscle glycogen content from 459 (83) to 565 (62) mmol.kg-1 dry weight (d.w.) (P < 0.05). However, despite the increased pre-exercise muscle glycogen stores, there was no difference in the distance cycled during the TT [40.41 (1.44) vs 40.18 (1.76) km for NORM and SUPP, respectively]. With NORM, muscle glycogen declined from 459 (83) to 175 (64) mmol.kg-1 d.w., whereas with SUPP the corresponding values were 565 (62) and 292 (113) mmol.kg-1 d.w. Accordingly, both muscle glycogen utilisation [277 (64) vs 273 (114) mmol.kg-1 d.w.] and total CHO oxidation [169 (20) vs 165 (30) g.h-1 for NORM and SUPP, respectively] were similar. Neither were there any differences in plasma glucose or lactate concentrations during the two experimental trials. Plasma glucose concentration averaged 5.5 (0.5) and 5.6 (0.6) mmol.l-1, while plasma lactate concentration averaged 4.4 (1.9) and 4.4 (2.3) mmol.l-1 for NORM and SUPP, respectively. The results of this study show that when well-trained subjects increase the CHO content of their diet for 3 days from 6 to 9 g.kg-1 BM there is only a modest increase in muscle glycogen content. Since supplementary CHO did not improve TT performance, we conclude that additional CHO provides no benefit to performance for athletes who compete in intense, continuous events lasting 1 h. Furthermore, the substantial muscle CHO reserves observed at the termination of exercise indicate that whole-muscle glycogen depletion does not determine fatigue at this exercise intensity and duration.

Adult↗

Effects of steady-state versus stochastic exercise on subsequent cycling performance.

The aims of this investigation were to evaluate the physiological responses to laboratory based stochastic exercise and to assess the effects of stochastic versus steady-state exercise on subsequent cycling time trial (TT) performance. Six competitive cyclists (peak power output (PPO) 432 +/- 39 W (values are mean +/- SD) undertook in a random order two 150-min paced rides that were either constant load (58% of PPO) or stochastic in nature (58 +/- 12.2% of PPO). These rides were immediately followed by a 20-km TT performance on an air-braked ergometer. Mean heart rate (HR) responses throughout the 150-min paced rides and during the subsequent TT were not significantly different between trials. Yet, despite the similarities in HR, the mean time for the TT was significantly faster (26:32 +/- 1:30 vs 28:08 +/- 1:47 min, P < 0.05) and the mean power output was significantly greater (340.3 +/- 44.2 vs 302.5 +/- 42.3 W; 77.8 +/- 10.2 vs 70.0 +/- 9.8% of PPO, P < 0.05) following the steady-state ride. These results demonstrate that following 150 min of steady-state riding, subsequent 20 km TT performance was significantly improved when compared with 150 min of stochastic exercise.

Adult↗

Assessment of the reproducibility of performance testing on an air-braked cycle ergometer.

The purposes of this study were (I) to assess the reproducibility of endurance performance testing on an air-braked cycle ergometer, and (II) to compare laboratory performances to performances in road races. Ten well-trained, competitive cyclists (peak power output [PPO] 443 +/- 37 W, [values are mean +/- SD]) undertook either: (I) three 20 km and three 40 km time trials (TT) on an air braked ergometry system (Kingcycle) (n = 6), and/or (II) three 40 km laboratory TT and two 40 km road TT competitions (n = 8). The time taken for the laboratory simulated 20 km and 40 km TT rides were highly reproducible (coefficient of variation 1.1 +/- 0.9% and 1.0 +/- 0.5%, respectively). However, the mean power output and heart rate were significantly different (p < 0.0001) between the 20 km and 40 km TT (327.5 +/- 16.9 vs 303.9 +/- 14.9 W and 171.4 +/- 5.1 vs 168.3 +/- 4.4 beats/min, respectively). A strong relationship (r = 0.99, p < 0.001) was observed between the mean cycling time and the average sustained power output. A significant correlation (r = 0.98, p < 0.001) was also observed between laboratory and road race times, although road race times were, on average, some 8% slower. These findings indicate that the Kingcycle ergometry system can be used as a reliable method of assessing short term endurance cycling performance.

Bicycling↗

Water ingestion does not improve 1-h cycling performance in moderate ambient temperatures.

Eight endurance-trained cyclists rode as far as possible in 1 h on a stationary cycle simulator in a moderate environment (20 degrees C, 60% relative humidity, 3 m.s-1 wind speed) while randomly receiving either no fluid (NF) or attempting to replace their approximate 1.71 sweat loss measured in a previous 1-h familiarisation performance ride at approximately 85% of peak oxygen uptake with artificially sweetened, coloured water (F). During F, the cyclists drank mean 1.49 (SEM 0.14) 1 of which mean 0.27 (SEM 0.08) 1 remained in the stomach at the end of exercise and mean 0.20 (SEM 0.05) 1 was urinated after the trial. Thus, only mean 1.02 (SEM 0.12) 1 of the ingested fluid was available to replace sweat losses during the 1-h performance ride. That fluid decreased the mean average heart rate from 166 (SEM 3) to 157 (SEM 5) beats.min-1 (P < 0.0001) and reduced the final mean serum [Na+] and osmolalities from 143 (SEM 0.6) to 139 (SEM 0.6) matom.l-1 (P < 0.005) and from 294 (SEM 1.7) to 290 (SEM 1.9) mosmol.l-1 (P = 0.05), respectively. Fluid ingestion did not significantly attenuate rises in plasma anti-diuretic hormone and angiotensin concentrations, or decrease the approximate-15% falls in estimated plasma volume in the F and NF trials. Nor did fluid ingestion significantly affect the approximate 1.71.h-1 sweat rates, the rises in rectal temperature (from 36.6 degrees to 38.3 degrees C) or the ratings of perceived exertion in the two trials.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Heart rate responses during a 4-d cycle stage race.

The purpose of this study was to monitor the heart rates (HR) of seven, well-trained (maximal oxygen uptake [VO2max] 5.0 +/- 0.5 l.min-1), competitive cyclists during a 4-d cycle stage race. On consecutive days, subjects competed in a 16.0-km individual time trial (TT), a 110.0-km mass-start road race (RR1), a 5.5-km individual hill climb (HC), and a 105.0-km mass-start road race (RR2). Within 10 d of the final race, cyclists underwent a test to determine VO2max, peak power output, and maximal HR. Comparison of the HR responses to each race revealed that the individual events were performed at a relatively high and constant work rate (91.1 +/- 2.5% and 93.2 +/- 4.7% of the maximal HR as measured in the field (HRmax) for the TT and HC, respectively). In contrast, despite similar racing speeds (42.2 +/- 1.0, 39.9 +/- 0.2, and 40.6 +/- 0.5 km.h-1 for the TT, RR1, and RR2, respectively), the HR responses to the longer mass-start races were reduced to 81.9 +/- 9.6% and 78.6 +/- 8.9% of HRmax and were random in frequency and amplitude. Such stochastic changes in HR were seemingly unrelated to course terrain but may be due to the group dynamics of the cyclists. The results of this study reveal the stochastic nature of bunch cycle racing and show that the HR responses of competitive cyclists are more a function of tactical bunch riding than of terrain.

Bicycling↗

Liposome-encapsulated-amikacin therapy of Mycobacterium avium complex infection in beige mice.

Efficacy of liposome-encapsulated amikacin and free amikacin against Mycobacterium avium complex was evaluated in the beige mouse (C57BL/6J-bgJ/bgJ) acute infection model. Approximately 10(7) viable M. avium complex serotype 1 cells for which the MIC of amikacin was 8 micrograms/ml were given intravenously. Treatment was started with encapsulated or free amikacin at approximately 110 or 40 mg/kg of body weight 7 or 14 days later. In the former experiment, treatment was given two or three times per week. In the latter experiment, treatment was given daily for 5 days. The animals were sacrificed 5 days after the last dose. Liver, spleen, and lung were homogenized, and viable cell counts were determined on 7H10 agar. An analysis of variance and subsequent Tukey HSD (honestly significant difference) tests indicated that both encapsulated and free amikacin significantly reduced viable cell counts in each of the organs compared with counts in the control group. Compared with free amikacin, encapsulated amikacin significantly reduced viable cell counts in the liver and spleen. Liposome encapsulation of an active agent appears to be a promising therapeutic approach to M. avium complex infection.

Amikacin↗

In-vitro susceptibility of Mycobacterium tuberculosis, Mycobacterium bovis and Mycobacterium kansasii to amoxycillin and ticarcillin in combination with clavulanic acid.

The in-vitro susceptibility of Mycobacterium tuberculosis, M. bovis, and M. kansasii to amoxycillin alone and in combination with 2 mg/l of clavulanic acid was evaluated by broth dilution. The MIC90 of amoxycillin plus clavulanic acid was 4 mg/l compared with greater than 32 mg/l for amoxycillin alone when tested against M. tuberculosis (n = 27). M. bovis (n = 8) was the most susceptible species with an MIC90 of amoxycillin 8 mg/l, compared with 0.5 mg/l for the combination. M. kansasii (n = 6), with an MIC90 of 16 mg/l for amoxycillin plus clavulanic acid was more resistant than either M. tuberculosis or M. bovis. Ticarcillin plus clavulanic acid with an MIC90 of 32 mg/l was less active against M. tuberculosis (n = 28) than amoxycillin plus clavulanic acid. The addition of clavulanic acid to amoxycillin greatly improves its in-vitro activity against M. tuberculosis and M. bovis.

Amoxicillin↗

Comparative in vitro activities of ampicillin, BMY 28142, and imipenem against Mycobacterium avium complex.

The in vitro activity of ampicillin, BMY 28142, and imipenem was evaluated against 21 clinical isolates of Mycobacterium avium complex by both a broth and an agar dilution method. The MIC90 by broth dilution for ampicillin, BMY 28142, and imipenem was 16 micrograms/ml, 8 micrograms/ml, and greater than 32 micrograms/ml, respectively. The MIC90 by agar dilution for ampicillin and BMY 28142 was 16 micrograms/ml.

Ampicillin↗

In vitro susceptibility of Mycobacterium fortuitum to amoxicillin or cephalothin in combination with clavulanic acid.

The comparative in vitro activity of cefoxitin, cephalothin, amoxicillin, and clavulanic acid in combination with the latter two agents against 13 isolates of Mycobacterium fortuitum was evaluated by agar dilution susceptibility testing. Amoxicillin was more active than cephalothin but less active than cefoxitin against the strains tested. Clavulanic acid in combination with these beta-lactams usually improved the activity by one or two dilutions compared with the beta-lactams alone.

Amoxicillin↗

In vitro activity of amoxicillin in combination with clavulanic acid against Mycobacterium tuberculosis.

The comparative in vitro activity of amoxicillin alone and in combination with clavulanic acid against 15 isolates of Mycobacterium tuberculosis was evaluated by broth dilution susceptibility testing. Amoxicillin inhibited 4 of 15 isolates at 8 micrograms/ml or less but was not bactericidal against any of the isolates at that concentration. Amoxicillin in combination with clavulanic acid was bactericidal for 14 of 15 isolates tested at an amoxicillin concentration of 4 micrograms/ml or less and a clavulanic acid concentration of 2 micrograms/ml or less.

Amoxicillin↗

In vitro susceptibility of Mycobacterium fortuitum to N-formimidoyl thienamycin and several cephamycins.

The comparative in vitro activity of N-formimidoyl thienamycin, cefmetazole, cefoxitin, cefotetan (YM-09330), and moxalactam against 13 isolates of Mycobacterium fortuitum was evaluated by agar dilution susceptibility testing. N-Formimidoyl thienamycin inhibited 10 to 12 strains at 6.25 micrograms/ml, cefmetazole inhibited 12 of 13 strains at 12.5 micrograms/ml, cefoxitin inhibited 11 of 13 strains at 25 micrograms/ml, and cefotetan inhibited 11 of 13 strains at 50 micrograms/ml. Moxalactam was less active than the other compounds tested, inhibiting only 9 of 13 strains at 50 micrograms/ml.

Anti-Bacterial Agents↗