Evidence of break-points in breathing pattern at the gas-exchange thresholds during incremental cycling in young, healthy subjects.

The present study investigated whether 'break-points' in breathing pattern correspond to the first ([Formula: see text]) and second gas-exchange thresholds ([Formula: see text]) during incremental cycling. We used polynomial spline smoothing to detect accelerations and decelerations in pulmonary gas-exchange data, which provided an objective means of 'break-point' detection without assumption of the number and shape of said 'break-points'. Twenty-eight recreational cyclists completed the study, with five individuals excluded from analyses due to low signal-to-noise ratios and/or high risk of 'pseudo-threshold' detection. In the remaining participants (n = 23), two separate and distinct accelerations in respiratory frequency (f (R)) during incremental work were observed, both of which demonstrated trivial biases and reasonably small ±95% limits of agreement (LOA) for the [Formula: see text] (0.2 ± 3.0 ml O(2) kg(-1) min(-1)) and [Formula: see text] (0.0 ± 2.4 ml O(2) kg(-1) min(-1)), respectively. A plateau in tidal volume (V (T)) data near the [Formula: see text] was identified in only 14 individuals, and yielded the most unsatisfactory mean bias ±LOA of all comparisons made (-0.4 ± 5.3 ml O(2) kg(-1) min(-1)). Conversely, 18 individuals displayed V (T)-plateau in close proximity to the [Formula: see text] evidenced by a mean bias ± LOA of 0.1 ± 3.1 ml O(2) kg(-1) min(-1). Our findings suggest that both accelerations in f (R) correspond to the gas-exchange thresholds, and a plateau (or decline) in V (T) at the [Formula: see text] is a common (but not universal) feature of the breathing pattern response to incremental cycling.

The influence of breathing mechanics on the development of the slow component of O2 uptake.

We examined the influence of operational lung volumes and mean inspiratory flow on the amplitude of the slow component of O2uptake (V(O)2(SC) ) during constant-load cycling performed below and above the respiratory compensation threshold (RCT) in young (24±1yr), healthy individuals (n=10). Subjects demonstrated a significantly greater rise in expiratory reserve volume (ERV) and mean inspiratory flow over the V(O)2(SC) period during exercise performed above compared with below the RCT (P<0.05). Inspiratory reserve volume (IRV) was, on average, smaller for trials performed above relative to below the RCT (P<0.05). The difference in the magnitudes of change in ERV and mean inspiratory flow, but not IRV, were positively correlated with the increase in V(O)2(SC) amplitude between work rates (R(2)=0.86, P<0.01). These findings suggest that dynamic hyperinflation and mean inspiratory flow (by increasing inspiratory resistive work) contribute to the development of the V(O)2(SC') , particularly when exercise is performed above the RCT.

Breathing He-O2 attenuates the slow component of O2 uptake kinetics during exercise performed above the respiratory compensation threshold.

The contribution of respiratory muscle O2 uptake ((.)V(O2RM)) to the development of the slow component of O2 uptake kinetics ((.)V(O2SC)) is unclear. The aim of the present study was to examine the impact of respiratory muscle unloading (via breathing, a He-O2 mixture) on the amplitude of (.)V(O2SC) during exercise performed below (B-RCT) and above the respiratory compensation threshold (A-RCT). We hypothesized that breathing He-O2 would reduce the amplitude of the (.)V(O2SC) by a greater amount during exercise performed A-RCT than B-RCT. Eight healthy male recreational cyclists performed constant load cycling in four sets of conditions: (1) B-RCT breathing normal air; (2) B-RCT breathing He-O2; (3) A-RCT breathing normal air; and (4) A-RCT breathing He-O2. Breathing He-O2 did not significantly attenuate the (.)V(O2SC) during exercise performed B-RCT (-3+/-14%, P >0.05). However, breathing He-O2 significantly reduced the (.)V(O2SC) during exercise A-RCT(-45+/-6%, P <0.05). The attenuated (.)V(O2SC) while breathing He-O2 is likely to reflect a decreased (.)V(O2RM). Minute ventilation was not +/-different between normal air and He-O2 breathing trials either B-RCT or A-RCT. However, operating lung volume was significantly lower when breathing He-O2 during exercise performed A-RCT (-12+/-3%, P <0.05). These findings suggest that (.)V(O2RM) comprises a greater proportion of the (.)V(O2SC) when exercise is performed A-RCT compared with B-RCT. Therefore, the impact of breathing He-O2 was more pronounced during exercise A-RCT. Furthermore, changes in operating lung volume and the work of breathing appear to play an important role in the development of the (.)V(O2SC).

Exercise-related change in airway blood flow in humans: relationship to changes in cardiac output and ventilation.

This study examined the relationship between airway blood flow (Q(aw)), ventilation (V(E)) and cardiac output (Q(tot)) during exercise in healthy humans (n=12, mean age 34+/-11 yr). Q(aw) was estimated from the uptake of the soluble gas dimethyl ether while V(E) and Q(tot) were measured using open circuit spirometry. Measurements were made prior to and during exercise at 34+/-5 W (Load 1) and 68+/-10 W (Load 2) and following the cessation of exercise (recovery). Q(aw) increased in a stepwise fashion (P<0.05) from rest (52.8+/-19.5 microl min(-1) ml(-1)) to exercise at Load 1 (67.0+/-20.3 microl min(-1) ml(-1)) and Load 2 (84.0+/-22.9 microl min(-1) ml(-1)) before returning to pre-exercise levels in recovery (51.7+/-13.2 microl min(-1) ml(-1)). Q(aw) was positively correlated with both Q(tot) (r=0.58, P<0.01) and V(E) (r=0.50, P<0.01). These results demonstrate that the increase in Q(aw) is linked to an exercise related increase in both Q(tot) and V(E) and may be necessary to prevent excessive airway cooling and drying.

Muscle glycogen reduction in man: relationship between surface EMG activity and oxygen uptake kinetics during heavy exercise.

The purpose of this study was to determine whether muscle glycogen reduction prior to exercise would alter muscle fibre recruitment pattern and change either on-transient O2 uptake (VO2) kinetics or the VO2 slow component. Eight recreational cyclists (VO2peak, 55.6 +/- 1.3 ml kg (-1) min(-1)) were studied during 8 min of heavy constant-load cycling performed under control conditions (CON) and under conditions of reduced type I muscle glycogen content (GR). VO2 was measured breath-by-breath for the determination of VO2 kinetics using a double-exponential model with independent time delays. VO2 was higher in the GR trial compared to the CON trial as a result of augmented phase I and II amplitudes, with no difference between trials in the phase II time constant or the magnitude of the slow component. The mean power frequency (MPF) of electromyography activity for the vastus medialis increased over time during both trials, with a greater rate of increase observed in the GR trial compared to the CON trial. The results suggest that the recruitment of additional type II motor units contributed to the slow component in both trials. An increase in fat metabolism and augmented type II motor unit recruitment contributed to the higher VO2 in the GR trial. However, the greater rate of increase in the recruitment of type II motor units in the GR trial may not have been of sufficient magnitude to further elevate the slow component when VO2 was already high and approaching VO2peak .

Lower limb vasodilatory capacity is not reduced in patients with moderate COPD.

We compared exercise capacity (peak O2 uptake; VO(2peak)) and lower limb vasodilatory capacity in 9 patients with moderate COPD (FEV1 52.7 +/- 7.6% predicted) and 9 age-matched healthy control subjects. VO(2peak) was measured via open circuit spirometry during incremental cycling. Calf blood flow (CBF) measurements were obtained at rest and after 5 minutes of ischemia using venous occlusion plethysmography. While VO(2peak) was significantly lower in the COPD patients (15.8 +/- 3.5 mL x kg(-1) x min(-1)) compared with the control group (25.2 +/- 3.5 mL x kg(-1) x min(-1)), there were no significant differences between groups in peak CBF or peak calf conductance measured 7 seconds post-ischemia. VO(2peak) was significantly correlated with peak CBF and peak conductance in the control group, whereas no significant relationship was found between these variables in the COPD group. However, the rate of decay in blood flow following ischemia was significantly slower (p < 0.05) for the COPD group (-0.036 +/- 0.005 mL x 100 mL(-1) x min(-1) x S(-1)) when compared with controls (-0.048 +/- 0.015 mL x 100 mL(-1) x min(-1) x S(-1)). The results suggest that the lower peak exercise capacity in patients with moderate COPD is not related to a loss in leg vasodilatory capacity.

The VO2 slow component: relationship between plasma ammonia and EMG activity.

PURPOSE: An increased recruitment of type II muscle fibers has been suggested as a major cause of the slow component of O(2) uptake (VO(2)) kinetics. Furthermore, the rise in plasma ammonia (NH(3)) during high-intensity exercise, where a slow component is observed, has been associated with the activation of type II muscle fibers. Therefore, the purpose of this study was to examine the relationship between the VO(2) slow component, plasma NH3 concentration, and electromyography (EMG) responses during constant-load cycling. METHODS: Eight healthy adults (mean age +/- SEM: 21.4 +/- 1.0 yr) performed 7 min of heavy constant-load exercise. The breath-by-breath VO(2) response was characterized using a two-term exponential model. Plasma NH(3) concentration was measured at rest, following 3 min of unloaded cycling and at 3 and 7 min of constant-load exercise. Surface EMG activity of the right vastus lateralis muscle was measured during the final 10 s of every minute of exercise. RESULTS: The amplitude of the slow component was 561 +/- 52 mL.min(-1), and occurred 132 +/- 11 s following the onset of constant-load exercise. Plasma NH(3) concentration increased significantly from 3 to 7 min of constant-load exercise by 32.2 +/- 2.9 micromol.L(-1). The rise in plasma NH(3) concentration correlated significantly with the amplitude of the slow component (r = 0.79, P < 0.05). The mean power frequency of the EMG increased significantly while the integrated EMG/VO(2) ratio remained constant over the duration of the slow component. CONCLUSION: The rise in NH(3) concentration and the amplitude and spectral components of the EMG are consistent with a progressive increase in the recruitment of type II muscle fibers during the slow component phase of exercise.

Maximal leg-strength training improves cycling economy in previously untrained men.

PURPOSE: This study examined cycling economy before and after 8 wk of maximal leg-strength training. METHODS: Seven previously untrained males (25 +/- 2 yr) performed leg-strength training 3 d.wk(-1) for 8 wk using four sets of five repetitions at 85% of one repetition maximum (1RM). Body mass, lean-leg muscle mass (LLM), percentage of body fat, and leg strength (1RM) were measured at 0, 4, and 8 wk of training. Cycling economy was calculated as the deltaVO2/deltaWR (change in the O2 cost of exercise divided by the change in the power between two different power outputs). RESULTS: There were significant increases in LLM and 1RM from 0 to 4 wk of training (LLM: 25.8 +/- 0.7 to 27.2 +/- 0.8 kg; 1RM: 138 +/- 9 to 215 +/- 9 kg). From 4 to 8 wk of training, 1RM continued to increase significantly (215 +/- 9 to 266 +/- 8 kg) with no further change observed in LLM. Peak power during incremental cycling increased significantly (305 +/- 14 to 315 +/- 16 W), whereas the power output achieved at the gas-exchange threshold (GET) remained unchanged. Peak O2 uptake and the O2 uptake achieved at the GET also remained unchanged following training. Cycling economy improved significantly when the power output was increased from below the GET to above the GET but not for power outputs below the GET. CONCLUSION: Maximal leg-strength training improves cycling economy in previously untrained subjects. Increases in leg strength during the final 4 wk of training with unchanged LLM suggest that neural adaptations were present.

Excess post-exercise oxygen consumption in spinal cord-injured men.

This study examined excess post-exercise oxygen consumption (EPOC) following arm cranking in men who had a traumatic spinal cord injury (SCI). Six physically active SCI men with a lesion level between T10 and T12 and six able-bodied (AB) men who were matched according to upper body peak VO(2) performed 30 min of arm-cranking at 65-70% peak VO(2). Baseline measurements were recorded during the last 10 min of a 40-min seated rest. Subjects remained seated during recovery for 40 min or until VO(2) returned to baseline, whichever was longer. Plasma lactate concentration was measured at rest, at the end of exercise, and at 10, 20 and 40 min of recovery. EPOC duration was not significantly different ( P>0.05) between SCI [23.2 (7.9) min; mean (SE)] and AB [35.0 (15.4) min] men, nor was there a significant group difference in EPOC magnitude [36.8 (7.8) kJ for SCI and 53.0 (22.8) kJ for AB]. There was no significant difference in recovery heart rate (HR) or respiratory exchange ratio (RER) between SCI and AB. However, HR measured at the end of the EPOC period was significantly elevated ( P<0.001) and RER significantly lower ( P<0.03) for both groups when compared to baseline. Lactate concentration was not significantly different between the groups at any sampling period. The findings suggest that physically active SCI men have a similar energy expenditure and time frame for recovery from arm crank exercise as their AB counterparts. Similar to what has been reported following lower body exercise, arm crank exercise elicits a higher HR and lower RER at end-EPOC when compared to pre-exercise values.

Oxygen uptake kinetics during severe exercise: a comparison between young and older men.

This study examined the relationship between the slow component of oxygen uptake (VO2) kinetics and muscle electromyography (EMG) during severe exercise in nine young (21.7+/-0.9 yr) and nine older (71.6+/-0.8 yr) men. Oxygen uptake (VO2) and surface EMG activity of the left vastus lateralis muscle were measured during a 7-min square-wave bout of severe exercise on a cycle ergometer. The absolute amplitude of the VO2 slow component was greater and occurred approximately 60 s earlier in the young compared to older subjects. However, the rate of increase in the slow component, expressed as a percentage of the total VO2 response per unit time, was not different between young and older subjects (young: 4.8+/-0.5%.min(-1); older: 4.9+/-0.6%.min(-1)). The mean power frequency (MPF) of the EMG increased significantly during the slow component phase of exercise by 6.4+/-1.0% in the young and by 5.4+/-0.7% in the older group and this rise was not significantly different between the two groups. These results indicate that normal ageing may not alter the VO2 slow component (measured as the rate of increase in VO2) and that this finding may be related to similar muscle fibre recruitment patterns in the two groups during severe-intensity exercise.

Oxygen uptake and heart rate kinetics during heavy exercise: a comparison between arm cranking and leg cycling.

This study examined the oxygen uptake (VO(2)) and heart rate (HR) kinetics during arm cranking and leg cycling at work rates above the anaerobic threshold (AT). Ten untrained male subjects [21.6 (1.3) years] completed two 7 min 15 s constant-load arm cranking and two leg cycling tests at a power output halfway between the mode-specific AT and peak VO(2). The time constants for phase II VO(2) (tau) and HR (tau) kinetics were determined by fitting a monoexponential curve from the end of phase I until 3 min of exercise. VO(2) tau and HR tau values were significantly (P < 0.001) slower in arm cranking [VO(2) tau = 66.4 (3.0) s; HR tau = 74.7 (4.4) s] than in leg cycling [VO(2) tau = 42.0 (1.9) s; HR tau = 55.6 (3.5) s]. The VO(2) slow component (VO(2SC)) accounted for a significantly (P < 0.001) greater percentage of the total exercise response during arm cranking [23.8 (1.6)%] than during leg cycling [14.2 (1.5)%]. The greater relative VO(2SC) and the slower VO(2) tau with arm exercise are consistent with a greater recruitment of metabolically inefficient type II muscle fibres during arm cranking than during leg cycling.

Increases in maximal accumulated oxygen deficit after high-intensity interval training are not gender dependent.

Gender differences in maximal accumulated oxygen deficit (MAOD) were examined before and after 4 and 8 wk of high-intensity interval training. Untrained men (n = 7) and women (n = 7) cycled at 120% of pretraining peak oxygen uptake (VO2 peak) to exhaustion (MAOD test) pre-, mid-, and posttraining. A posttraining timed test was also completed at the MAOD test power output, but this test was stopped at the time to exhaustion achieved during the pretraining MAOD test. The 14.3 +/- 5.2% increase in MAOD observed in men after 4 wk of training was not different from the 14.0 +/- 3.0% increase seen in women (P > 0.05). MAOD increased by a further 6.6 +/- 1.9% in men, and this change was not different from the additional 5.1 +/- 2.3% increase observed in women after the final 4 wk of training. VO2 peak measured during incremental cycling increased significantly (P < 0.01) in male but not in female subjects after 8 wk of training. Moreover, the accumulated oxygen (AO2) uptake was higher in men during the posttraining timed test compared with the pretraining MAOD test (P < 0.01). In contrast, the AO2 uptake was unchanged from pre- to posttraining in female subjects. The increase in MAOD with training was not different between men and women, suggesting an enhanced ability to produce ATP anaerobically in both groups. However, the increase in VO2 peak and AO2 uptake obtained in male subjects after training indicates improved oxidative metabolism in men but not in women. We conclude that there are basic gender differences that may predispose men and women to specific metabolic adaptations after a period of intense interval training.