Controlled-frequency breath swimming improves swimming performance and running economy.

Respiratory muscle fatigue can negatively impact athletic performance, but swimming has beneficial effects on the respiratory system and may reduce susceptibility to fatigue. Limiting breath frequency during swimming further stresses the respiratory system through hypercapnia and mechanical loading and may lead to appreciable improvements in respiratory muscle strength. This study assessed the effects of controlled-frequency breath (CFB) swimming on pulmonary function. Eighteen subjects (10 men), average (standard deviation) age 25 (6) years, body mass index 24.4 (3.7) kg/m(2), underwent baseline testing to assess pulmonary function, running economy, aerobic capacity, and swimming performance. Subjects were then randomized to either CFB or stroke-matched (SM) condition. Subjects completed 12 training sessions, in which CFB subjects took two breaths per length and SM subjects took seven. Post-training, maximum expiratory pressure improved by 11% (15) for all 18 subjects (P < 0.05) while maximum inspiratory pressure was unchanged. Running economy improved by 6 (9)% in CFB following training (P < 0.05). Forced vital capacity increased by 4% (4) in SM (P < 0.05) and was unchanged in CFB. These findings suggest that limiting breath frequency during swimming may improve muscular oxygen utilization during terrestrial exercise in novice swimmers.

The association of the distance walked in 6 min with pre-operative peak oxygen consumption and complications 1 month after colorectal resection.

We measured the distance 112 patients walked in 6 min, as well as their peak oxygen consumption pedalling a bicycle, week before scheduled resection of benign or malignant colorectal disease. The distance walked correlated with peak oxygen consumption, the former 'accounting' for about half the variation in the latter, r² 0.52 (95% CI 0.38-0.64), p < 0.0001. In the first postoperative month, 42/112 patients experienced a complication. In multivariate analysis, complications were less likely with longer walking distances and increasing age: the odds ratio (95% CI) reduced to 0.995 (0.990-0.999) for each metre distance, and to 0.96 (0.93-0.99) with each year of age, p = 0.025 and p = 0.018, respectively. The distance walked in 6 min before surgery can provide prognostic information when cardiopulmonary exercise testing is unavailable.

Pulmonary diffusion and aerobic capacity: is there a relation? Does obesity matter?

AIM: We sought to determine whether pulmonary diffusing capacity for nitric oxide (DLNO), carbon monoxide (DLCO) and pulmonary capillary blood volume (Vc) at rest predict peak aerobic capacity (VO2peak), and if so, to discern which measure predicts better. METHODS: Thirty-five individuals with extreme obesity (body mass index or BMI = 50 +/- 8 kg m((-2)) and 26 fit, non-obese subjects (BMI = 23 +/- 2 kg m((-2)) participated. DLNO and DLCO at rest were first measured. Then, subjects performed a graded exercise test on a cycle ergometer to determine (VO2peak). Multivariate regression was used to assess relations in the data. RESULTS: Findings indicate that (i) pulmonary diffusion at rest predicts (VO2peak) in the fit and obese when measured with DLNO, but only in the fit when measured with DLCO; (ii) the observed relation between pulmonary diffusion at rest and (VO2peak) is different in the fit and obese; (iii) DLNO explains (VO2peak) better than DLCO or Vc. The findings imply the following reference equations for DLNO: (VO2peak) (mL kg(-1) min(-1)) = 6.81 + 0.27 x DLNO for fit individuals; (VO2peak) (mL kg(-1) min(-1)) = 6.81 + 0.06 x DLNO, for obese individuals (in both groups, adjusted R(2 )=( )0.92; RMSE = 5.58). CONCLUSION: Pulmonary diffusion at rest predicts (VO2peak), although a relation exists for obese subjects only when DLNO is used, and the magnitude of the relation depends on gender when either DLCO or Vc is used. We recommend DLNO as a measure of pulmonary diffusion, both for its ease of collection as well as its tighter relation with (VO2peak).

Exercise capacity of children with pediatric lung disease.

BACKGROUND: Pulmonary function of children with cystic fibrosis (CF) and bronchopulmonary dysplasia (BPD) is similar at rest even though the mechanisms of injury differ. We sought to compare the peak exercise responses in children with BPD versus CF while controlling for pulmonary impairment, nutritional status, gender, age, height, and predicted forced expired volume in 1 second (approximately 73% of predicted). METHODS: Nine BPD children and 9 CF children underwent spirometry and a progressive exercise test to maximum on a cycle ergometer. RESULTS: There was no difference between groups in body mass percentile (CF:97 +/- 13%, BPD: 98 +/- 11%), peak power output (Wpeak) (CF:67 +/- 19 W, BPD:73 +/- 28 W), % predicted Wpeak (CF:83 +/- 28%, BPD:88 +/- 15%), peak oxygen uptake (VO2peak, CF: 38 +/- 7 ml/kg/min, BPD: 39 +/-6 ml/kg/min), or % predicted VO2peak (CF:99 +/- 16 %, BPD:96 +/- 27%). CONCLUSIONS: Children with mild pulmonary impairments are able to achieve a near normal peak power output and a normal VO2peak. Neither the aetiology nor the developmental onset of the process appears to be important influences on VO2peak or Wpeak.

Pulmonary gas exchange in the morbidly obese.

The literature on pulmonary gas exchange at rest, during exercise, and with weight loss in the morbidly obese (body mass index or BMI > or = 40 kg m(-2)) is reviewed. Forty-one studies were found (768 subjects weighted mean = 40 years old, BMI = 48 kg m(-2)). The alveolar-to-arterial oxygen partial pressure difference (AaDO2) was large at rest in upright subjects at sea level (23, range 5-38 mmHg) while the arterial pressure of oxygen (PaO2) was low (81, range 50-95 mmHg). Arterial pressure of carbon dioxide (PaCO2) was normal. At peak exercise (162 W), gas exchange improves. Weight loss of 45 kg (BMI = -13 kg m(-2)) over 18 months is associated with an improvement in PaO2 (by 10 mmHg, range 1-23 mmHg), a reduction in AaDO2 (by 8 mmHg, range -3 to -16 mmHg), and PaCO2 (by -3 mmHg, range 3 to -14 mmHg) at rest. Every 5-6 kg reduction in weight increases PaO2 by 1 and reduces AaDO2 by 1 mmHg, respectively. Morbidly obese women have better gas exchange at rest compared with morbidly obese men which is likely due to lower waist-to-hip ratios in women than from differences in weight or BMI.

Laboratory 20-km cycle time trial reproducibility.

This study evaluated the reproducibility of laboratory based 20-km time trials in well trained versus recreational cyclists. Eighteen cyclists (age = 34 +/- 8 yrs; body mass index = 23.1 +/- 2.2 kg/m (2); VO(2max) = 4.19 +/- 0.65 L/min) completed three 20-km time trials over a month on a Velotron cycle ergometer. Average power output (PO) (W), speed, and heart rate (HR) were significantly lower in the first time trial compared to the second and third time trial. The coefficients of variation (CV) between the second and third trial of the top eight performers for average PO, time to completion, and speed were 1.2 %, 0.6 %, 0.5 %, respectively, compared to 4.8 %, 2.0 %, and 2.3 % for the bottom ten. In addition, the average HR, VO(2), and percentage of VO(2max) were similar between trials. This study demonstrated that (1) a familiarization session improves the reliability of the measurements (i.e., average PO, time to completion and speed), and (2) the CV was much smaller for the best performers.

Evidence of pulmonary oedema triggered by exercise in healthy humans and detected with various imaging techniques.

This review summarizes current literature on pulmonary oedema triggered by above-ground exercise in healthy humans from studies that use various imaging techniques to detect oedema. Eleven studies were identified, comprising of 137 subjects (mean age = 28 years). Eighty per cent (n = 110) were males, and 20% (n = 27) were female. The studies were grouped into three different categories according to the severity of the exercise protocol, which were either prolonged, submaximal exercise of 15-min to 2 h in duration at approx. 50-75%VO(2max) and not to exhaustion (PROLONGED, n = 44), a VO(2max) test lasting 16-20 min in which the intensity of exercise was only maximum for about 2 min at the end of the test (GXT, n = 15), and maximum or near maximum effort exercise protocols at or near volitional exhaustion where the goal was to finish in the fastest possible time or maintain the highest possible workload (MAX EFFORT, n = 78). Only 16% of the subjects showed signs of oedema from PROLONGED exercise and no subjects (0%) showed signs of oedema from GXT exercise. Surprisingly, approx. 65% of the subjects showed signs of oedema triggered by MAX EFFORT exercise (chi(2) test of association; P < or = 0.01), which was independent of both sex, the level of hypoxia (inspired PO(2) = 106-118 mmHg vs. 149 mmHg), the timing of the post-exercise imaging (<10, >30 but <60 min, or >60 min) and VO(2max) (approx. 3.0 vs. approx. 4.8 L min(-1)). The data suggests that the chances of triggering pulmonary oedema from exhaustive MAX EFFORT exercise is 4x more compared with PROLONGED exercise. As well, the likelihood of triggering pulmonary oedema may be independent of lung size, sex, moderate levels of hypoxia, and aerobic fitness.

A small amount of inhaled nitric oxide does not increase lung diffusing capacity.

The aim of the present study was to determine: 1) whether 40-50 ppm nitric oxide (NO) increases diffusing capacity of the lung for NO (D(L,NO)) and carbon monoxide (D(L,CO)), membrane diffusing capacity for CO (D(m,CO)) and pulmonary capillary blood volume (V(c)); 2) the actual number of tests required to provide a reasonable estimate of D(L,NO), D(L,CO), D(m,CO) and V(c); and 3) repeatability of these parameters using the single-breath D(L,NO)-D(L,CO) method. In total, 31 subjects performed five single-breath hold manoeuvres at rest, inhaling 43+/-3 ppm NO together with a standard diffusion mixture. D(L,NO) (D(m,CO)) remained unchanged from the first to fifth trial. However, compared with the first trial, D(L,CO) and V(c) had decreased by the fourth (-4+/-5%; 95% confidence interval (CI) = -5- -2%) and third trial (-5+/-7%; 95% CI = -7- -2%), respectively. Repeatability over five trials was 17, 3 and 7 mL.min(-1).mmHg(-1) for D(L,NO), D(L,CO) and D(m,CO), respectively, and 13 mL for V(c) when D(m,CO) = D(L,NO)/2.42. In conclusion, nitric oxide inhaled during sequential single-breath manoeuvres has no effect on diffusing capacity of the lung for nitric oxide and, thus, membrane diffusing capacity for carbon monoxide. Since more than two and three trials will lower pulmonary capillary blood volume and diffusing capacity of the lung for carbon monoxide, respectively, the average value of only two properly performed trials is suggested.

Red cell pulmonary transit times through the healthy human lung.

It has previously been postulated that rapid red cell capillary transit through the human lung plays a role in the mechanism of diffusion limitation in some endurance athletes. Methodological limitations currently prevent researchers from directly measuring pulmonary capillary transit times in humans during exercise; however, first pass radionuclide cardiography allows direct measurement of red blood cell (RBC) transit times through the whole lung at various exercise intensities. We examined the relationship between mean whole lung red cell pulmonary transit times (cardiopulmonary transit times or CPTT) and different levels of flow in 88 healthy humans (76 males, 12 females) from several studies (mean age 31 years). The pooled data suggest that the relationship between CPTT and cardiac index (CI), beginning at rest and progressing through to maximum exercise demonstrates that CPTT reaches its minimum value when CI is about 8.1 l m2 x min(-1) (2.5-3 times the CI value at rest), and does not significantly change with further increases in CI. Cardiopulmonary blood volume (CPBV) index also does not change significantly until CI reaches 2.5 to 3 times the CI value at rest and then increases roughly linearly after that point. Consequently, the systematic increase in CPBV index with increasing pulmonary blood flow between 8.1 and 20 l m2 x min(-1) displays an adaptive response of the cardiopulmonary system by augmenting CPBV (and perhaps pulmonary capillary blood volume through distension and recruitment) to offset the reduction in CPTT, as no significant difference in mean CPTT is observed between these levels of flow (P > 0.05). Therefore, these data demonstrate that CPBV does not reach maximum capacity during strenuous or maximum exercise. This does not support the principle of quarter-power allometric scaling for flow when explaining modifications during exercise. Therefore, we speculate that the observed relationships between CPTT, CBPV index and flow may prevent mean CPTT (and perhaps mean pulmonary capillary transit times) from decreasing below the threshold time required for oxygenation.

Acute hypervolemia lengthens red cell pulmonary transit time during exercise in endurance athletes.

The purpose was to determine if acute plasma volume expansion (PVE) changed red-cell pulmonary transit time (PTT) during severe exercise. Twelve endurance athletes performed 6.5 min of severe cycling exercise on different days. Pentaspan [(500 ml, infusion condition, I] or placebo [(60 ml saline), non-infusion condition, N] were infused prior to exercise. Blood gas tensions, PTT, multigated acquisition (MUGA) derived cardiac output, and oxygen uptake were measured during exercise. PTT was measured during minute 3 of exercise by radionuclide cardiography. Arterial P(O(2)) (Pa(O(2))), and alveolar-arterial oxygen pressure difference (AaD(O(2))) at minute 3 of exercise did not differ between conditions. Mean PTT at minute 3 of exercise was 0.3 sec longer in the I condition (P=0.002). However, the change in PTT between conditions was not correlated to the change in either Pa(O(2)) or AaD(O(2)). We conclude that PVE slows (lengthens) PTT without affecting pulmonary gas exchange. Therefore, rapid PTT may not be related to hypoxemia during exercise.

Acute effects of intense interval training on running mechanics.

The aims of this study were to determine if there are significant kinematic changes in running pattern after intense interval workouts, whether duration of recovery affects running kinematics, and whether changes in running economy are related to changes in running kinematics. Seven highly trained male endurance runners (VO2max = 72.3+/-3.3 ml x kg(-1) x min(-1); mean +/- s) performed three interval running workouts of 10 x 400 m at a speed of 5.94+/-0.19 m x s(-1) (356+/-11.2 m x min(-1)) with a minimum of 4 days recovery between runs. Recovery of 60, 120 or 180 s between each 400 m repetition was assigned at random. Before and after each workout, running economy and several kinematic variables were measured at speeds of 3.33 and 4.47 m x s(-1) (200 and 268 m x min(-1)). Speed was found to have a significant effect on shank angle, knee velocity and stride length (P < 0.05). Correlations between changes pre- and post-test for VO2 (ml x kg(-1) x min(-1)) and several kinematic variables were not significant (P > 0.05) at both speeds. In general, duration of recovery was not found to adversely affect running economy or the kinematic variables assessed, possibly because of intra-individual adaptations to fatigue.

Evidence and possible mechanisms of altered maximum heart rate with endurance training and tapering.

Exercise physiologists, coaches and athletes have traditionally used heart rate (HR) to monitor training intensity during exercise. While it is known that aerobic training decreases submaximal HR (HRsubmax) at a given absolute exercise workload, the general consensus is that maximum HR (HRmax) is relatively unaltered regardless of training status in a given population. It has not been seriously postulated as to whether HRmax can change modestly with aerobic training/detraining. Despite several sources stating that HRmax is unaltered with training, several studies report that HRmax is reduced following regular aerobic exercise by sedentary adults and endurance athletes, and can increase upon cessation of aerobic exercise. Furthermore, evidence suggests that tapering/detraining can increase HRmax. Therefore, it is plausible that some of the same mechanisms that affect both resting and HRsubmax may also play a role in altered HRmax. Some of the proposed mechanisms for changes in HRmax that may occur with aerobic training include autonomic (extrinsic) factors such as plasma volume expansion and(enhanced baroreflex function, while some nonautonomic (intrinsic) factors are alteration of the electrophysiology of the sinoatrial (SA) node and decreased beta-adrenergic receptor number and density. There is a high correlation between changes in both maximal oxygen uptake (VO2 max) and HRmax that occurs with training, tapering and detraining (r= -0.76: p < 0.0001; n = 314), which indicates that as VO2max improves with training, HRmax tends to decrease, and when detraining ensues, HRmax tends to increase. The overall effect of aerobic training and detraining on HRmax is moderate: effect sizes based on several studies were calculated to be -0.48 and +0.54, respectively. Therefore, analysis reveals that HRmax can be altered by 3 to 7% with aerobic training/detraining. However, because of a lack of research in the area of training on HRmax, the reader should remain speculative and allow for cautious interpretation until further, more thorough investigations are carried out as to the confirmation of mechanisms involved. Despite the limitations of using HR and HRmax as a guide to training intensity, the practical implications of monitoring changing HRmax are: (i) prescribed training intensities may be more precisely monitored; and (ii) prevention of overtraining may possibly be enhanced. As such, it may be sensible to monitor HRmax directly in athletes throughout the training year, perhaps at every macrocycle (3 to 6 weeks).

Effect of intense interval workouts on running economy using three recovery durations.

The purposes of this study were to determine whether running economy (RE) is adversely affected following intense interval bouts of 10 x 400-m running, and whether there is an interaction effect between RE and recovery duration during the workouts. Twelve highly trained male endurance athletes [maximal oxygen consumption; VO2max = 72.5 (4.3) ml x kg(-1) x min(-1) mean (SD)] performed three interval running workouts of 10 x 400 m with a minimum of 4 days between runs. Recovery duration between the repetitions was randomly assigned at 60, 120 or 180 s. The velocity for each 400-m run was determined from a treadmill VO2max test. The average running velocity was 357.9 (9.0) m x min(-1). Following the workout, the rating of perceived exertion (RPE) increased significantly (P < 0.01) as recovery duration between the 400-m repetitions decreased (14.4, 16.1, and 17.7 at 180s, 120s, and 60 s recovery, respectively). Prior to and following each workout, RE was measured at speeds of 200 and 268 m x min(-1). Changes in RE from pre- to post-workout, as well as heart rate (HR) and respiratory exchange ratio (R) were similar for the three recovery conditions. When averaged across conditions, oxygen consumption (VO2) increased significantly (P < 0.01) from pre- to post-test [from 38.5 to 40.5 ml x kg(-1) x min(-1) at 200 m x min(-1), and from 53.1 to 54.5 ml x kg(-1) x min(-1) at 268 m x min(-1), respectively]. HR increased (from 124 to 138, and from 151 to 157 beats x min(-1) respectively) and R decreased (from 0.90 to 0.78, and from 0.93 to 0.89, respectively) at 200 and 268 m x min(-1), respectively (P < 0.01). This study showed that RE can be perturbed after a high-intensity interval workout and that the changes in VO2, HR and R were independent of the recovery duration between the repetitions.