Canadian journal of applied physiology = Revue canadienne de physiologie appliquee最新文献

Background: I/D polymorphism of the ACE gene may be associated with better endurance performance and a stronger response to exercise training. The aim of this study was to investigate the association between ACE gene polymorphism and athletic performance in a homogeneous cohort.

Methods: Eighty-eight male non-elite Caucasian Turkish athletes with similar training backgrounds for at least for 6 months were studied for ACE gene polymorphisms by PCR analysis. Performance on the 60-meter sprint and middle-distance running tests were evaluated.

Results: The distributions of the ACE I/D genotypes were 20.5%, 40.9%, and 38.6% for II, ID, and DD polymorphisms in the whole group (N = 88), respectively. The ACE DD genotype frequency was significantly higher in the superior group (56.7%) than in the poor (37.9%) and mediocre (20.7%) group in middle-distance running performance (chi2 = 11.778; p = 0.019).

Conclusion: The ACE DD genotype may be related to better short-duration aerobic endurance performance. Larger homogeneous cohorts may help clarify the association between ACE I/D polymorphism and physical performance.

Objective: This two-part study tested the hypotheses that the use of a new cooling device, purported to extract heat from the body core through the palm of the hand, would (a) attenuate core temperature rise during submaximal exercise in the heat, thereby suppressing exercise-associated metabolic changes, and (b) facilitate a higher sustained workload, thus shortening the completion time of a time-trial performance test.

Methods: In Study 1, 8 male triathletes (age 27.9 +/- 2.0 yrs, mass 77.2 +/- 3.1 kg, VO2peak 59.0 +/- 4.1 ml x min(-1) x kg(-1)) cycled for 1 hr at the same absolute workload (approximately 60% VO2peak) in a heated room (31.9 +/- 0.1 degrees C, 24 +/- 1% humidity) on two occasions counterbalanced for cooling (C) or noncooling (NC). In Study 2, 8 similar subjects (age 26.9 +/- 2.0 yrs, mass 75.2 +/- 3.7 kg, VO2peak 54.1 +/- 3.1 ml x min(-1) x kg(-1)) performed two 30-km cycling time-trial performance tests under the same conditions (C(T), NC(T)).

Results: In Study 1, cooling attenuated the rise in tympanic temperature (T(TY)) (1.2 +/- 0.2 vs. 1.8 +/- 0.2 degrees C; p < 0.01) and lowered mean oxygen consumption (VO2, 2.4 +/- 0.1 vs. 2.7 +/- 0.1 L x min(-1); p < 0.05) and blood lactate (1.7 +/- 0.2 vs. 2.2 +/- 0.2 mmol x L(-1); p < 0.01) during exercise. There were no significant differences in respiratory exchange ratio (RER), blood glucose, heart rate (HR), face temperature (T(F)), or back temperature (T(B)) between NC and C. In Study 2, time to complete 30 km was 6 +/- 1% less with cooling than without cooling (60.9 +/- 2.0 vs. 64.9 +/- 2.6 min; p < 0.01). During the last 20% of C(T), subjects sustained a workload that was 14 +/- 5% (p = 0.06) higher than NC(T) at the same T(TY) and HR.

Conclusions: Heat extraction through the hand during cycle ergometer exercise in the heat can (a) lower T(TY), lactate concentration, and VO2 during a submaximal set-workload test and (b) reduce the time it takes to complete a 30-km time-trial test.

The following study was conducted to evaluate the hypothesis that an increase in the postexercise onset threshold for cutaneous vasodilation (Th(VD)) and sweating (Th(SW)) would not be observed upon the restoration of baseline mean arterial pressure (MAP). Subjects remained either seated resting for 15 min or performed 15 min of treadmill running at 70% VO2peak followed by either 20- (short) or 60-min (extended) recovery. At the end of each recovery protocol (20 and 60 min) a water perfusion suit was then used to increase mean skin temperature until Th(VD) and Th(SW) was noted. Exercise resulted in an increase in Th(VD) and Th(SW) of 0.24 +/- 0.03 and 0.24 +/- 0.02 degrees C, respectively, above no-exercise for the short recovery (p < 0.05). No increase was measured for the extended recovery. Postexercise MAP was significantly reduced prior to whole-body warming for the short recovery whereas no reduction was measured for the extended recovery. The increase in Th(VD) and Th(SW), measured during the early stages of recovery, is reversed with the reestablishment of baseline MAP.

The objective of this study was to determine differences in electromyographic (EMG) activity of the soleus (SOL), vastus lateralis (VL), biceps femoris (BF), abdominal stabilizers (AS), upper lumbar erector spinae (ULES), and lumbo-sacral erector spinae (LSES) muscles while performing squats of varied stability and resistance. Stability was altered by doing the squat movement on a Smith machine, a free squat, and while standing on two balance discs. Fourteen male subjects performed the movements. Activities of the SOL, AS, ULES, and LSES were highest during the unstable squat and lowest with the Smith machine protocol (p < 0.05). Increased EMG activity of these muscles may be attributed to their postural and stabilization role. Furthermore, EMG activity was higher during concentric contractions compared to eccentric contractions. Performing squats on unstable surfaces may permit a training adaptation of the trunk muscles responsible for supporting the spinal column (i.e., erector spinae) as well as the muscles most responsible for maintaining posture (i.e., SOL).

The purpose of the study was to (a) assess the effects of sodium citrate ingestion on metabolism and performance capacity in a 5-km competitive outdoor stadium run in trained male runners, and (b) elucidate the potential relationship between citrate-induced changes in plasma volume, body mass, and performance. Ten subjects (age 22.1 +/- 2.5 yrs, body mass 74.1 +/- 6.1 kg, height 180.1 +/- 5.7 cm, (.)VO(2)max 60.8 +/- 5.5 ml x kg(-1) x min(-1)) participated in the study. There was no effect of treatment on 5-km running time: 1100.0 +/- 79.1 and 1082.7 +/- 62.0 s in citrate (CIT) and in placebo (PLC) trials, respectively, p = 0.09. Blood pH increased from 7.34 +/- 0.07 to 7.49 +/- 0.07 (p = 0.002) as a result of administering sodium citrate in the amount of 0.5 g x kg(-1) body mass in 1.5 litres of solution but remained stable while the equal volume of placebo drink was consumed: 7.40 +/- 0.04 and 7.44 +/- 0.09. The relative change in plasma volume after administering the drink was -1.99 +/- 3.49% in the PLC and 9.75 +/- 6.51% in the CIT trial (p = 0.001). Body mass did not differ before drinking; however, before the start the subjects were heavier in the CIT trial (74.2 +/- 6.1 kg) vs. the PLC trial (73.4 +/- 6.2 kg, p = 0.048). The shifts in plasma volume and body mass were not related to changes in performance. The results suggest that ingestion of sodium citrate induces an increase in water retention, plasma volume, and blood pH before exercise but does not improve performance in a 5-km competitive run in field conditions in trained male runners.

The purpose of this study was to examine the effect of a 5-day creatine (CR) supplementation period on red blood cell (RBC) CR uptake in vegetarian and nonvegetarian young women. Blood samples were collected from lacto-ovo vegetarians (VG, n = 6, age 21.8 +/- 1.9 yrs) and nonvegetarians (NV, n = 6, age 21.7 +/- 1.9 yrs) before and after a 5-day CR loading period (0. 3g CR/kg lean body mass/day), and from a control group of nonvegetarians (NV, n = 5, age 22.0 +/- 0.7 yrs) who did not supplement with creatine. RBC and plasma samples were analyzed for the presence of creatine. Significant increases (p < .05) in RBC and plasma CR levels were found for vegetarians and nonvegetarians following supplementation. The initial RBC CR content was significantly lower (p < .05) in the vegetarian group. There was no significant difference between vegetarians and nonvegetarians in final RBC CR content, suggesting that a ceiling had been reached. As the uptake into both muscle and RBC is moderated by creatine transporter proteins, analysis of the uptake of CR into RBC may reflect the uptake of CR into muscle, offering an alternative to biopsies.

Homocysteine is a sulfur-containing amino acid that arises during methionine metabolism. Although its concentration in plasma is only about 10 micromolar, even moderate hyperhomocysteinemia is associated with increased incidence of cardiovascular disease and Alzheimer's disease. Elevations in plasma homocysteine are commonly found as a result of vitamin deficiencies, polymorphisms of enzymes of methionine metabolism, and renal disease. Pyridoxal, folic acid, riboflavin, and Vitamin B(12) are all required for methionine metabolism, and deficiency of each of these vitamins result in elevated plasma homocysteine. A polymorphism of methylenetetrahydrofolate reductase (C677T), which is quite common in most populations with a homozygosity rate of 10-15 %, is associated with moderate hyperhomocysteinemia, especially in the context of marginal folate intake. Plasma homocysteine is inversely related to plasma creatinine in patients with renal disease. This is due to an impairment in homocysteine removal in renal disease. The role of these factors, and of modifiable lifestyle factors, in affecting methionone metabolism and in determining plasma homocysteine levels is discussed.

The metabolic syndrome comprises an array of cardiovascular disease (CVD) risk factors such as abdominal obesity, dyslipidemia, hypertension, and glucose intolerance. Insulin resistance and/or increased abdominal (visceral) obesity have been suggested as potential etiological factors. More recently, increasing evidence has associated insulin resistance and subclinical inflammation involving cytokines derived from adipose tissue, or adipocytokines. Despite the fact that precise mechanisms have yet to be established, there is a significant role for both diet and physical activity to improve the many factors associated with the metabolic syndrome, including modulation of various adipocytokines. Although both diet and physical activity have been studied for their ability to modify cytokines in more traditional inflammatory conditions, such as rheumatoid arthritis, they have been less studied in relation to inflammation as an underlying cause of the metabolic syndrome and/or CVD. A more thorough understanding of the clustering of metabolic abnormalities and their underlying etiology will help to define diet and physical activity guidelines for preventing and treating the metabolic syndrome, an important aspect of CVD prevention. This paper will address potential underlying causes of the metabolic syndrome, with a focus on the putative mechanistic role of adipocytokines, and will discuss the impact of diet and physical activity on the metabolic syndrome.

The present study was designed to investigate the heart rate-running speed (HR-RS) relationship while exercising continuously, at high intensities, on a treadmill. The purpose was to precisely measure the magnitude of drop in RS necessary to maintain HR during intense exhaustive exercises, and to determine whether the magnitude of drop in RS is directly dependent on exercise intensity. Sixteen male endurance athletes performed five treadmill tests: an incremental test for maximal O2 uptake and maximum aerobic velocity (VMA), and four exhaustive tests: at 82, 86, 89, and 92 % VMA. After an adaptation period of 3 min, the objective was to stabilise HR by adjusting the treadmill speed continuously by +/- 0.5 km x h(-1) every 30 sec. Attained intensities were: 82 % (+/-6), 84 % +/- (6), 89 % (+/-3), and 90 % (+/-6) VMA, respectively [L1, L2] vs. [L3, L4], p < 0.05. Time to exhaustion across the increasing intensities, respectively, were: 36.58 (+/-4.45), 24.63 (+/-3.25), 15.80 (+/-2.00), and 9.87 (+/-1.15) min, p < 0.05, with the exception of L3 vs. L4. The RS/HR ratio vs. speed showed three phases: an increasing adaptive (AB) phase 0-165 sec with an averaging maximal level of 1.67 m x beat(-1) at 165 sec, a transitional period 170-245 sec, and a decreasing (BC) phase 250-1800 sec with a lower level of 1.29 m .beat(-1) at 1800 sec. In our experimental conditions, for high intensities 82 to 90 % VMA, cardiac drift which disturbed the RS-HR relationship with duration was evaluated: -0.143 km x h(-1) per minute for HR stabilisation. This cardiac drift is a linear function of time. Results suggest that HR and RS are not interchangeable variables for this kind of exercises, and it seems more reliable to gauge exercise intensity using RS than HR.