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The lactate threshold (LT), critical power (CP) and maximum oxygen uptake ( $$\dot{V}{\text{O}}_{2\text{max} }$$ ) together partition exercise intensity domains by their common physiological, biochemical and perceptual response characteristics. CP is the greatest power output attainable immediately following intolerance at $$\dot{V}{\text{O}}_{{2{\text{peak}}}}$$ , and the asymptote of 3 min all-out exercise. Thus we reasoned that a maximal ‘sprint’ immediately following standard ramp-incremental exercise would allow characterisation of the three aerobic indices in a single test. Ten healthy men (23 ± 3 year, mean ± SD) performed 9 cycle-ergometry tests on different days: (A) two ramp-incremental tests to intolerance (20 W min−1), immediately followed by a 3 min maximal, variable-power effort ramp-sprint test (RST) for LT, $$\dot{V}{\text{O}}_{{2{\text{peak}}}}$$ and sprint-phase power (SP) determination; (B) four constant-power tests for CP and $$\dot{V}{\text{O}}_{2\text{max} }$$ determination; (C) constant-power tests at 10 W below LT, and 10 W below and above SP to verify intensity domain characterisation. Capillary [lactate] and breath-by-breath $$\dot{V}{\text{O}}_{2}$$ were measured. Reproducibility of LT, SP and $$\dot{V}{\text{O}}_{2\text{max} }$$ measurements between RST repeats was within 5 % or less (r ≥ 0.991, p

The mechanism for slow pulmonary O2uptake (V̇o2) kinetics in patients with chronic heart failure (CHF) is unclear but may be due to limitations in the intramuscular control of O2utilization or O2delivery. Recent evidence of a transient overshoot in microvascular deoxygenation supports the latter. Prior (or warm-up) exercise can increase O2delivery in healthy individuals. We therefore aimed to determine whether prior exercise could increase muscle oxygenation and speed V̇o2kinetics during exercise in CHF. Fifteen men with CHF (New York Heart Association I–III) due to left ventricular systolic dysfunction performed two 6-min moderate-intensity exercise transitions ( bouts 1 and 2, separated by 6 min of rest) from rest to 90% of lactate threshold on a cycle ergometer. V̇o2was measured using a turbine and a mass spectrometer, and muscle tissue oxygenation index (TOI) was determined by near-infrared spectroscopy. Prior exercise increased resting TOI by 5.3 ± 2.4% ( P = 0.001), attenuated the deoxygenation overshoot (−3.9 ± 3.6 vs. −2.0 ± 1.4%, P = 0.011), and speeded the V̇o2time constant (τV̇o2; 49 ± 19 vs. 41 ± 16 s, P = 0.003). Resting TOI was correlated to τV̇o2before ( R2= 0.51, P = 0.014) and after ( R2= 0.36, P = 0.051) warm-up exercise. However, the mean response time of TOI was speeded between bouts in half of the patients (26 ± 8 vs. 20 ± 8 s) and slowed in the remainder (32 ± 11 vs. 44 ± 16 s), the latter group having worse New York Heart Association scores ( P = 0.042) and slower V̇o2kinetics ( P = 0.001). These data indicate that prior moderate-intensity exercise improves muscle oxygenation and speeds V̇o2kinetics in CHF. The most severely limited patients, however, appear to have an intramuscular pathology that limits V̇o2kinetics during moderate exercise.

During exercise below the lactate threshold (LT), the rate of adjustment (τ) of pulmonary VO(2) uptake (τ) is slowed when initiated from a raised work rate. Whether this is consequent to the intrinsic properties of newly recruited muscle fibres, slowed circulatory dynamics or the effects of a raised metabolism is not clear. We aimed to determine the influence of these factors on τV(O(2)) using combined in vivo and in silico approaches. Fifteen healthy men performed repeated 6 min bouts on a cycle ergometer with work rates residing between 20 W and 90% LT, consisting of the following: (1) two step increments in work rate (S1 and S2), one followed immediately by the other, equally bisecting 20 W to 90% LT; (2) two 20 W to 90% LT bouts separated by 30 s at 20 W to raise muscle oxygenation and pretransition metabolism (R1 and R2); and (3) two 20 W to 90% LT bouts separated by 12 min at 20 W allowing full recovery (F1 and F2). Pulmonary O(2) uptake was measured breath by breath by mass spectrometry and turbinometry, and quadriceps oxygenation using near-infrared spectroscopy. The influence of circulatory dynamics on the coupling of muscle and τV(O(2)) lung was assessed by computer simulations. The τV(O(2)) in R2 (32 ± 9 s) was not different (P > 0.05) from S2 (30 ± 10 s), but both were greater (P < 0.05) than S1 (20 ± 10 s) and the F control bouts (26 ± 10 s). The slowed V(O(2)) kinetics in R2 occurred despite muscle oxygenation being raised throughout, and could not be explained by slowed circulatory dynamics (τV(O(2)) predicted by simulations: S1 = R2 < S2). These data therefore suggest that the dynamics of muscle O(2) consumption are slowed when exercise is initiated from a less favourable energetic state.

Tolerance to high-intensity constant-power (P) exercise is well described by a hyperbola with two parameters: a curvature constant (W′) and power asymptote termed “critical power” (CP). Since the ability to sustain exercise is closely related to the ability to meet the ATP demand in a steady state, we reasoned that pulmonary O2 uptake (V̇o2) kinetics would relate to the P-tolerable duration (tlim) parameters. We hypothesized that 1) the fundamental time constant (τV̇o2) would relate inversely to CP; and 2) the slow-component magnitude (ΔV̇o2sc) would relate directly to W′. Fourteen healthy men performed cycle ergometry protocols to the limit of tolerance: 1) an incremental ramp test; 2) a series of constant-P tests to determine V̇o2max, CP, and W′; and 3) repeated constant-P tests (WR6) normalized to a 6 min tlim for τV̇o2 and ΔV̇o2sc estimation. The WR6 tlim averaged 365 ± 16 s, and V̇o2max (4.18 ± 0.49 l/min) was achieved in every case. CP (range: 171–294 W) was inversely correlated with τV̇o2 (18–38 s; R2 = 0.90), and W′ (12.8–29.9 kJ) was directly correlated with ΔV̇o2sc (0.42–0.96 l/min; R2 = 0.76). These findings support the notions that 1) rapid V̇o2 adaptation at exercise onset allows a steady state to be achieved at higher work rates compared with when V̇o2 kinetics are slower; and 2) exercise exceeding this limit initiates a “fatigue cascade” linking W′ to a progressive increase in the O2 cost of power production (V̇o2sc), which, if continued, results in attainment of V̇o2max and exercise intolerance. Collectively, these data implicate V̇o2 kinetics as a key determinant of high-intensity exercise tolerance in humans.

Laboratory-based studies have demonstrated that adding protein (PRO) to a carbohydrate (CHO) supplement can improve thermoregulatory capacity, exercise performance and recovery. However, no study has investigated these effects in a competitive sporting context. This study assessed the effects of combined CHO-PRO supplementation on physiological responses and exercise performance during 8 days of strenuous competition in a hot environment. Twenty-eight cyclists participating in the TransAlp mountain bike race were randomly assigned to fitness-matched placebo (PLA 76 g L(-1) CHO) or CHO-PRO (18 g L(-1) PRO, 72 g L(-1) CHO) groups. Participants were given enough supplements to allow ad libitum consumption. Physiological and anthropometric variables were recorded pre- and post-exercise. Body mass decreased significantly from race stage 1 to 8 in the PLA group (-0.75 ± 0.22 kg, P = 0.01) but did not change in the CHO-PRO group (0.42 ± 0.42 kg, P = 0.35). Creatine kinase concentration and muscle soreness were substantially elevated during the race, but were not different between groups (P = 0.82, P = 0.44, respectively). Urine osmolality was significantly higher in the CHO-PRO versus the PLA group (P = 0.04) and the rise in tympanic temperature from pre- to post-exercise was significantly less in CHO-PRO versus PLA (P = 0.01). The CHO-PRO group also completed the 8 stages significantly quicker than the PLA group (2,277 ± 127 vs. 2,592 ± 68 min, respectively, P = 0.02). CHO-PRO supplementation therefore appears to prevent body mass loss, enhance thermoregulatory capacity and improve competitive exercise performance despite no effect on muscle damage.

Objective— Circulating progenitor cells (CPC) have emerged as potential mediators of vascular repair. In experimental models, CPC mobilization is critically dependent on nitric oxide (NO). South Asian ethnicity is associated with reduced CPC. We assessed CPC mobilization in response to exercise in Asian men and examined the role of NO in CPC mobilization per se. Methods and Results— In 15 healthy, white European men and 15 matched South Asian men, CPC mobilization was assessed during moderate-intensity exercise. Brachial artery flow-mediated vasodilatation was used to assess NO bioavailability. To determine the role of NO in CPC mobilization, identical exercise studies were performed during intravenous separate infusions of saline, the NO synthase inhibitor l -NMMA, and norepinephrine. Flow-mediated vasodilatation (5.8%±0.4% vs 7.9%±0.5%; P =0.002) and CPC mobilization (CD34 + /KDR + 53.2% vs 85.4%; P =0.001; CD133 + /CD34 + /KDR + 48.4% vs 73.9%; P =0.05; and CD34 + /CD45 − 49.3% vs 78.4; P =0.006) was blunted in the South Asian group. CPC mobilization correlated with flow-mediated vasodilatation and l -NMMA significantly reduced exercise-induced CPC mobilization (CD34 + /KDR + −3.3% vs 68.4%; CD133 + /CD34 + /KDR + 0.7% vs 71.4%; and CD34 + /CD45 − −30.5% vs 77.8%; all P Conclusion— In humans, NO is critical for CPC mobilization in response to exercise. Reduced NO bioavailability may contribute to imbalance between vascular damage and repair mechanisms in South Asian men.

to the editor: We thank Dr. Francescato and colleagues for their interest in our study ([1][1]) and for their letter ([3][2]). The authors requested clarification of why we concluded that 1-s interpolation of breath-by-breath pulmonary oxygen uptake (Vo2P) data resulted in the most accurate and

During constant-power high-intensity exercise, the expected increase in oxygen uptake (V̇O2) is supplemented by a V̇O2 slow component (V̇O2 sc ), reflecting reduced work efficiency, predominantly within the locomotor muscles. The intracellular source of inefficiency is postulated to be an increase in the ATP cost of power production (an increase in P/W). To test this hypothesis, we measured intramuscular ATP turnover with (31)P magnetic resonance spectroscopy (MRS) and whole-body V̇O2 during moderate (MOD) and heavy (HVY) bilateral knee-extension exercise in healthy participants (n = 14). Unlocalized (31)P spectra were collected from the quadriceps throughout using a dual-tuned ((1)H and (31)P) surface coil with a simple pulse-and-acquire sequence. Total ATP turnover rate (ATPtot) was estimated at exercise cessation from direct measurements of the dynamics of phosphocreatine (PCr) and proton handling. Between 3 and 8 min during MOD, there was no discernable V̇O2 sc (mean ± SD, 0.06 ± 0.12 l min(-1)) or change in [PCr] (30 ± 8 vs. 32 ± 7 mm) or ATPtot (24 ± 14 vs. 17 ± 14 mm min(-1); each P = n.s.). During HVY, the V̇O2 sc was 0.37 ± 0.16 l min(-1) (22 ± 8%), [PCr] decreased (19 ± 7 vs. 18 ± 7 mm, or 12 ± 15%; P 0.05) and ATPtot increased (38 ± 16 vs. 44 ± 14 mm min(-1), or 26 ± 30%; P 0.05) between 3 and 8 min. However, the increase in ATPtot (ΔATPtot) was not correlated with the V̇O2 sc during HVY (r(2) = 0.06; P = n.s.). This lack of relationship between ΔATPtot and V̇O2 sc , together with a steepening of the [PCr]-V̇O2 relationship in HVY, suggests that reduced work efficiency during heavy exercise arises from both contractile (P/W) and mitochondrial sources (the O2 cost of ATP resynthesis; P/O).

Constant work rate (CWR) exercise testing is highly responsive to therapeutic interventions and reveals physiological and functional benefits. No consensus exists, however, regarding optimal methods for selecting the pre-intervention work rate. We postulate that a CWR whose tolerated duration (t(lim)) is 6 minutes (WR6) may provide a useful interventional study baseline. WR6 can be extracted from the power-duration relationship, but requires 4 CWR tests. We sought to develop prediction algorithms for easier WR6 identification using backward stepwise linear regression, one in 69 COPD patients (FEV1 45 +/- 15% pred) and another in 30 healthy subjects (HLTH), in whom cycle ergometer ramp incremental (RI) and CWR tests with t(lim) of similar to 6 minutes had been performed. Demographics, pulmonary function, and RI responses were used as predictors. We validated these algorithms against power-duration measurements in 27 COPD and 30 HLTH (critical power 43 +/- 18W and 231 +/- 43W; curvature constant 5.1 +/- 2.7 kJ and 18.5 +/- 3.1 kJ, respectively). This analysis revealed that, on average, only corrected peak work rate (= WRpeak-1 min x WRslope) in RI was required to predict WR6 (COPD SEE = 5.0W; HLTH SEE = 5.6W; R-2 > 0.96; p

During exercise below the lactate threshold (LT), the rate of adjustment (τ) of pulmonary VO(2) uptake (τ) is slowed when initiated from a raised work rate. Whether this is consequent to the intrinsic properties of newly recruited muscle fibres, slowed circulatory dynamics or the effects of a raised metabolism is not clear. We aimed to determine the influence of these factors on τV(O(2)) using combined in vivo and in silico approaches. Fifteen healthy men performed repeated 6 min bouts on a cycle ergometer with work rates residing between 20 W and 90% LT, consisting of the following: (1) two step increments in work rate (S1 and S2), one followed immediately by the other, equally bisecting 20 W to 90% LT; (2) two 20 W to 90% LT bouts separated by 30 s at 20 W to raise muscle oxygenation and pretransition metabolism (R1 and R2); and (3) two 20 W to 90% LT bouts separated by 12 min at 20 W allowing full recovery (F1 and F2). Pulmonary O(2) uptake was measured breath by breath by mass spectrometry and turbinometry, and quadriceps oxygenation using near-infrared spectroscopy. The influence of circulatory dynamics on the coupling of muscle and τV(O(2)) lung was assessed by computer simulations. The τV(O(2)) in R2 (32 ± 9 s) was not different (P0.05) from S2 (30 ± 10 s), but both were greater (P0.05) than S1 (20 ± 10 s) and the F control bouts (26 ± 10 s). The slowed V(O(2)) kinetics in R2 occurred despite muscle oxygenation being raised throughout, and could not be explained by slowed circulatory dynamics (τV(O(2)) predicted by simulations: S1 = R2S2). These data therefore suggest that the dynamics of muscle O(2) consumption are slowed when exercise is initiated from a less favourable energetic state.

The physiological equivalents of the curvature constant (W′) of the high-intensity power-duration (P-tLIM) relationship are poorly understood, although they are presumed to reach maxima/minima at exhaustion. In an attempt to improve our understanding of the determinants of W′, we therefore aimed to determine its recovery kinetics following exhaustive exercise (which depletes W′) concomitantly with those of O2 uptake (V̇o2, a proxy for the kinetics of phosphocreatine replenishment) and blood lactate concentration ([L−]). Six men performed cycle-ergometer exercise to tLIM: a ramp and four constant-load tests, at different work rates, for estimation of lactate threshold, W′, critical power (CP), and maximum V̇o2. Three further exhausting tests were performed at different work rates, each preceded by an exhausting “conditioning” bout, with intervening recoveries of 2, 6, and 15 min. Neither prior exhaustion nor recovery duration altered V̇o2 or [L−] at tLIM. Postconditioning, the P-tLIM relationship remained well characterized by a hyperbola, with CP unchanged. However, W′ recovered to 37 ± 5, 65 ± 6, and 86 ± 4% of control following 2, 6, and 15 min of intervening recovery, respectively. The W′ recovery was curvilinear [interpolated half time ( t1/2) = 234 ± 32 s] and appreciably slower than V̇o2 recovery ( t1/2 = 74 ± 2 s) but faster than [L−] recovery ( t1/2 = 1,366 ± 799 s). This suggests that W′ determines supra-CP exercise tolerance, its restitution kinetics are not a unique function of phosphocreatine concentration or arterial [L−], and it is unlikely to simply reflect a finite energy store that becomes depleted at tLIM.

Background Circulating progenitor cells (CPCs) have emerged as potential mediators of vascular repair. In experimental models CPC mobilisation is critically dependent on nitric oxide (NO). South Asian ethnicity is associated with reduced CPCs; we assessed CPC mobilisation in response to exercise in Asian men and examined the role of NO in CPC mobilisation per se. Methods In 15 healthy white European men and 15 matched South Asian men, CPC mobilisation (relative % increase from pre- to post-exercise) was assessed during moderate intensity exercise using flow cytometry. Three subsets of CPCs were studied (CD34+/KDR+, CD133+/CD34+/KDR+ or CD34+/CD45−) and were expressed as a % of circulating lymphocytes). Brachial artery flow mediated vasodilatation (FMD) was used to assess NO bioavailability. To determine the role of NO in CPC mobilisation, identical exercise studies were performed during intravenous separate infusions of saline, the NO synthase inhibitor L-NMMA, and norepinephrine. Results Groups were well matched for age, blood pressure, indices of obesity and circulating lipids; however the South Asian group exhibited insulin resistance as measured by the HOMA-IR score (1.3±0.2 vs 0.8±0.1; p=0.047). FMD (5.8±0.4% vs 7.9±0.5%; p=0.002) and basal CPC numbers (CD34+/KDR+: 0.030% vs 0.046%, p=0.05; CD133+/CD34+/KDR+: 0.008% vs 0.014%, p=0.026; CD34+/CD45−: 0.011% vs 0.018%, p=0.044) were lower in the South Asian group. CPC mobilisation (CD34+/KDR+ 53.2% vs 85.4%, p=0.001; CD133+/CD34+/KDR+ 48.4% vs 73.9%, p=0.05; CD34+/CD45− 49.3% vs 78.4, p=0.006) was blunted in the South Asian group. CPC mobilisation correlated with FMD and L-NMMA significantly reduced exercise induced CPC mobilisation (CD34+/KDR+ −3.3% vs 68.4%; CD133+/CD34+/KDR+ 0.7% vs 71.4%; CD34+/CD45− −30.5% vs 77.8%; all p Conclusions In humans NO is critical for CPC mobilisation in response to exercise. Reduced NO bioavailability may contribute to imbalance between vascular damage and repair mechanisms in South Asian men. This project was supported by the British Heart Foundation.