Whey or Casein Hydrolysate with Carbohydrate for Metabolism and Performance in Cycling.

The protein type most suitable for ingestion during endurance exercise is undefined. This study compared co-ingestion of either 15 g/h whey or casein hydrolysate with 63 g/h fructose: maltodextrin (0.8:1) on exogenous carbohydrate oxidation, exercise metabolism and performance. 2 h postprandial, 8 male cyclists ingested either: carbohydrate-only, carbohydrate-whey hydrolysate, carbohydrate-casein hydrolysate or placebo-water in a crossover, double-blind design during 2 h of exercise at 60%W max followed by a 16-km time trial. Data were evaluated by magnitude-based inferential statistics. Exogenous carbohydrate oxidation, measured from (13)CO2 breath enrichment, was not substantially influenced by co-ingestion of either protein hydrolysate. However, only co-ingestion of carbohydrate-casein hydrolysate substantially decreased (98% very likely decrease) total carbohydrate oxidation (mean±SD, 242±44; 258±47; 277±33 g for carbohydrate-casein, carbohydrate-whey and carbohydrate-only, respectively) and substantially increased (93% likely increase) total fat oxidation (92±14; 83±27; 73±19 g) compared with carbohydrate-only. Furthermore, only carbohydrate-casein hydrolysate ingestion resulted in a faster time trial (-3.6%; 90% CI: ±3.2%) compared with placebo-water (95% likely benefit). However, neither protein hydrolysate enhanced time trial performance when compared with carbohydrate-only. Under the conditions of this study, ingesting carbohydrate-casein, but not carbohydrate-whey hydrolysate, favourably alters metabolism during prolonged moderate-strenuous cycling without substantially altering cycling performance compared with carbohydrate-only.

Whole body vibration increases hip bone mineral density in road cyclists.

This study aimed to determine the effects of 10 weeks of whole body vibration training on the bone density of well-trained road cyclists. 15 road cyclists were assigned to either a vibrating group (n=8), who undertook 15 min of intermittent whole body vibration at 30 Hz, 3 times per week while continuing with their normal cycling training; or a control group (n=7), who continued with their normal cycling training for the 10-week period. Cyclists were age, body mass and height matched with 15 sedentary participants. At baseline, all participants underwent regional dual x-ray absorptiometry scans, where both cycling groups had lower pelvic (p<0.050) and higher head bone mineral density (p<0.050) than the sedentary participants with no other differences observed. After 10 weeks of training, vibrating cyclists showed a significantly greater increase in hip bone mineral density (0.020±0.010 g.cm - 2 (1.65%), p=0.024) while the control cyclists ( - 0.004±0.001 g.cm - 2 (0%)) showed no change (p>0.050). The control group had a significantly lower spine bone mineral density (1.027±0.140 g.cm - 2, p=0.020) compared to baseline (1.039±0.140 g.cm - 2). This loss was not observed in the vibrating group. 10 weeks of whole body vibration training increased hip and preserved spine bone mineral density in road cyclists.

A comparison of the indirect estimate of mean arterial pressure calculated by the conventional equation and calculated to compensate for a change in heart rate.

The standard equation used to calculate mean arterial pressure (MAP) assumes that diastole persists for 2/3 and systole for 1/3 of each cardiac cycle. This ratio is altered when heart rate increases, and therefore we investigated the efficacy of predicting MAP during exercise using non-invasive indirect methods. Eight subjects exercised on a cycle ergometer for 3 minute intervals to elicit heart rates between 100-110, 120-130, 140-150, 160-170, and 180-190 beats/min. In the last minute of each 3 min interval an ECG recording was taken and systolic (SP) and diastolic (DP) blood pressure was measured by manual auscultation. MAP was calculated for each heart rate interval by: MAP=DP+1/3(SP-DP) (method A), and MAP= DP + Fs(SP- DP) (method B), where Fs is the fraction of the cardiac cycle comprising systole, measured from the ECG. Fs increased from 0.35+/-0.049 at rest to 0.47+/-0.039 at a heart rate of 180-190 beats/min. MAP measured by method B was consistently greater than MAP calculated by method A at all heart rates greater than resting heart rate (p<0.01). The error incurred when using the standard MAP equation (method A) to derive MAP during exercise (measured as the percentage difference between method A and B) increased linearly with heart rate (r=0.98). The standard MAP equation should not be applied during exercise, as it does not account for the change in the systolic: diastolic period ratio as heart rate increases.

Plasma lactate decline during passive recovery from high-intensity exercise.

PURPOSE: An athlete's ability to repeatedly perform at high intensities during intermittent exercise could be related to an accelerated plasma lactate removal ability during recovery periods. METHODS: We determined the decline in plasma lactate levels during passive recovery after an incremental exercise test to exhaustion on a bicycle ergometer in five trained and five untrained male subjects. Venous blood samples were taken during exercise and recovery for the analysis of plasma lactate concentration. The endurance fitness of the subjects was characterized using a variable known as the maximum turn point power output (MTP), measured in W x kg(-1). MTP describes the workload at which lactate levels rise significantly above resting concentrations. RESULTS: The decline in plasma lactate levels during recovery was determined at selected intervals from the exponential recovery curve plotted as a percentage of peak plasma lactate versus time. No significant relationships were found between the recovery parameters measured from the curve and the MTP values of these subjects (Spearman's rank order correlation; r(s) values from -0.042 to -0.31). CONCLUSIONS: Therefore, we can conclude that training confers no advantage to the decline in plasma lactate while recovering passively from exercise at equivalent relative maximal work intensities.

Evaluation of miniature data loggers for body temperature measurement during sporting activities.

We recorded body temperatures in four runners, two squash players and one swimmer at 1-min intervals using miniature data loggers. These single-channel loggers are small and light (25 g), and were easily carried by the athletes during their sporting activities. Wide-range loggers (-37 degrees C to +46 degrees C), which had a temperature resolution of 0.4 degrees C, were used to measure thigh skin temperature. Auditory canal temperature and rectal temperature were measured with narrow-range loggers (+34 degrees C to + 46 degrees C) which had a considerably higher resolution (0.04 degrees C). With the aid of visual analogue scales subjects reported that the thermometric equipment caused very little discomfort or impairment of exercise performance. Loggers connected to uncoated bead thermistors (used for skin and auditory canal temperatures) had a thermal time constant of 0.4 s, and that of the coated thermistors (rectal probes) was 6 s. We were able to waterproof the equipment and measure rectal temperature in a swimmer. Hot (35 degrees C) or cold (5 degrees C) ambient temperatures had an insignificant effect on the intrinsic accuracy of the data loggers, even when used without recalibration at those temperatures. We believe that miniature temperature loggers are convenient and accurate thermometers for use during sporting activities and may provide new insights into thermoregulation during exercise.

Reduced cardiac stiffness following exercise is associated with preserved myocardial collagen characteristics in the rat.

We determined whether the increment in cardiac end-diastolic compliance (a reduced diastolic stiffness constant) following endurance training is related to alterations in myocardial collagen characteristics. Sixteen weeks of habitual exercise (Ex) in rats, which produced left ventricular (LV) hypertrophy (LVH) [LV weight in g: Ex = 1.01 (0.04), sedentary control = 0.89 (0.04); P < 0.05], resulted in a reduced LV end-diastolic (LVED) chamber stiffness [slope of the linearised LVED pressure versus LVED internal diameter relation in kPa x mm(-1): Ex = 0.67 (0.03), control = 0.80 (0.03); P < 0.05]. The increased LVED chamber distensibility was associated with an attenuated myocardial stiffness [slope of the linearised LVED stress versus strain relation in g x cm(-2); Ex= 15 (3), control = 25 (2); P < 0.05]. Although LV total collagen content (mg) was increased in the exercised rats [Ex = 5.0 (0.3), control = 4.1 (0.2); P < 0.05], this was a reflection of the presence of LVH, as the myocardial collagen concentration (microg x mg(-1) LV wet weight) was unaltered [Ex = 4.9 (0.2), control = 4.6 (0.2)]. Furthermore, habitual exercise did not influence the percentage of myocardial collagen extracted following cyanogen bromide digestion (an index of collagen cross-linking), [i.e. Ex = 38 (3), control = 38 (3)], nor the proportion of myocardial collagen phenotypes I and III [I/III; Ex = 3.04 (0.20), control = 2.85 (0.22)]. In conclusion, exercise-induced increments in end-diastolic myocardial distensibility are unlikely to be a consequence of alterations in the properties of myocardial collagen.