Purpose
This study examined the relationship of physiological and anthropometric characteristics with parameters of the critical power (CP) model, and in particular the reconstitution of
W
′ ...following successive bouts of maximal exercise, amongst trained and untrained cyclists.
Methods
Twenty male adults (trained nine; untrained 11; age 39 ± 15 year; mass 74.7 ± 8.7 kg;
V̇
O
2max
58.0 ± 8.7 mL kg
−1
min
−1
) completed three incremental ramps (20 W min
−1
) to exhaustion interspersed with 2-min recoveries. Pearson’s correlation coefficients were used to assess relationships for
W
′ reconstitution after the first recovery (
W
′
rec1
), the delta in
W
′ reconstituted between recoveries (∆
W
′
rec
)
,
CP and
W
′.
Results
CP was strongly related to
V̇
O
2max
for both trained (
r
= 0.82) and untrained participants (
r
= 0.71), whereas
W
′ was related to
V̇
O
2max
when both groups were considered together (
r
= 0.54).
W
′
rec1
was strongly related to
V̇
O
2max
for the trained (
r
= 0.81) but not untrained (
r
= 0.18); similarly, ∆
W
′
rec
was strongly related to
V̇
O
2max
(
r
= − 0.85) and CP (
r
= − 0.71) in the trained group only.
Conclusions
Notable physiological relationships between parameters of aerobic fitness and the measurements of
W
′ reconstitution were observed, which differed among groups. The amount of
W
′ reconstitution and the maintenance of
W
′ reconstitution that occurred with repeated bouts of maximal exercise were found to be related to key measures of aerobic fitness such as CP and
V̇
O
2max
. This data demonstrates that trained cyclists wishing to improve their rate of
W
′ reconstitution following repeated efforts should focus training on improving key aspects of aerobic fitness such as
V̇
O
2max
and CP.
Purpose
The purpose of the present study was to determine whether a contiguous ramp and all-out exercise test could accurately determine critical power (CP) in a single laboratory visit during both ...upright and supine cycle exercise.
Methods
Healthy males completed maximal ramp-incremental exercise on a cycle ergometer in the upright (
n
= 15) and supine positions (
n
= 8), with task failure immediately followed by a 3-min all-out phase for determination of end-test power (EP). On separate days, participants undertook four constant-power tests in either the upright or supine positions with the limit of tolerance ranging from ~ 2 to 15 min for determination of CP.
Results
During upright exercise, EP was highly correlated with (
R
2
= 0.93,
P
< 0.001) and not different from CP (CP = 221 ± 40 W vs. EP = 226 ± 46 W,
P
= 0.085, 95% limits of agreement − 30, 19 W). During supine exercise, EP was also highly correlated with (
R
2
= 0.94,
P
< 0.001) and not different from CP (CP = 140 ± 42 W vs. EP = 136 ± 40 W,
P
= 0.293, 95% limits of agreement − 16, 24 W).
Conclusion
The present data suggest that EP derived from a contiguous ramp all-out exercise test is not different from the gold-standard method of CP determination during both upright and supine cycle exercise when assessed at the group level. However, the wide limits of agreement observed within the present study suggest that EP and CP should not be used interchangeably.
Purpose
The aim of this study was to investigate the individual
W
′
reconstitution kinetics of trained cyclists following repeated bouts of incremental ramp exercise, and to determine an optimal ...mathematical model to describe
W
′
reconstitution.
Methods
Ten trained cyclists (age 41 ± 10 years; mass 73.4 ± 9.9 kg;
V
˙
O
2
max
58.6 ± 7.1 mL kg min
−1
) completed three incremental ramps (20 W min
−1
) to the limit of tolerance with varying recovery durations (15–360 s) on 5–9 occasions.
W
′
reconstitution was measured following the first and second recovery periods against which mono-exponential and bi-exponential models were compared with adjusted
R
2
and bias-corrected Akaike information criterion (AICc).
Results
A bi-exponential model outperformed the mono-exponential model of
W
′
reconstitution (AICc 30.2 versus 72.2), fitting group mean data well (adj
R
2
= 0.999) for the first recovery when optimised with parameters of fast component (FC) amplitude = 50.67%; slow component (SC) amplitude = 49.33%; time constant (
τ
)
FC
= 21.5 s;
τ
SC
= 388 s. Following the second recovery,
W
′ reconstitution reduced by 9.1 ± 7.3%, at 180 s and 8.2 ± 9.8% at 240 s resulting in an increase in the modelled
τ
SC
to 716 s with
τ
FC
unchanged. Individual bi-exponential models also fit well (adj
R
2
= 0.978 ± 0.017) with large individual parameter variations (FC amplitude 47.7 ± 17.8%; first recovery: (
τ
)
FC
= 22.0 ± 11.8 s; (
τ
)
SC
= 377 ± 100 s; second recovery: (
τ
)
FC
= 16.3.0 ± 6.6 s; (
τ
)
SC
= 549 ± 226 s).
Conclusions
W′ reconstitution kinetics were best described by a bi-exponential model consisting of distinct fast and slow phases. The amplitudes of the FC and SC remained unchanged with repeated bouts, with a slowing of W′ reconstitution confined to an increase in the time constant of the slow component.
Purpose
We tested the hypothesis that incremental ramp cycling exercise performed in the supine position (
S
) would be associated with an increased reliance on muscle deoxygenation (deoxyheme) in ...the deep and superficial
vastus lateralis
(VLd and VLs, respectively) and the superficial
rectus femoris
(RFs) when compared to the upright position (
U
).
Methods
11 healthy men completed ramp incremental exercise tests in
S
and
U
. Pulmonary
V
˙
O
2
was measured breath-by-breath; deoxyheme was determined via time-resolved near-infrared spectroscopy in the VLd, VLs and RFs.
Results
Supine exercise increased the overall change in deoxyheme from baseline to maximal exercise in the VLs (
S
: 38 ± 23 vs.
U
: 26 ± 15 μM,
P
< 0.001) and RFs (
S
: 36 ± 21 vs.
U
: 25 ± 15 μM,
P
< 0.001), but not in the VLd (
S
: 32 ± 23 vs.
U
: 29 ± 26 μM,
P
> 0.05).
Conclusions
The present study supports that the impaired balance between O
2
delivery and O
2
utilization observed during supine exercise is a regional phenomenon within superficial muscles. Thus, deep muscle defended its O
2
delivery/utilization balance against the supine-induced reductions in perfusion pressure. The differential responses of these muscle regions may be explained by a regional heterogeneity of vascular and metabolic control properties, perhaps related to fiber type composition.
The purpose of the present study was to investigate the effect of ischemic preconditioning (IPC) on the recovery of exercise performance following maximal, incremental exercise. A total of 13 healthy ...males volunteered to participate, undertaking three experimental trials involving a constant work-rate bout of severe intensity exercise undertaken to the limit of tolerance that was preceded by a 40-min recovery period consequent to a maximal, incremental exercise test. During the recovery period, participants underwent IPC at 220 mmHg, sham IPC (SHAM; 20 mmHg), and passive rest (CON). Exercise tolerance time was higher following IPC as compared to SHAM and CON {199 ± 36 (CON) vs. 203 ± 35 (SHAM) vs. 219 ± 34 (IPC), p = 0.03}. This effect was accompanied by a tendency toward an augmented increase in blood lactate from rest to exercise in IPC compared to SHAM and CON (p = 0.08). There was no effect of IPC on oxygen uptake kinetics or muscle oxygenation as indicated via near-infrared spectroscopy. IPC may therefore have the capacity to augment recovery from prior maximal exercise, but this does not appear to be due to enhancements to oxygen uptake kinetics or muscle oxygenation.
New Findings
What is the central question of this study?
Critical power is a fundamental parameter defining high‐intensity exercise tolerance and is related to the phase II time constant of pulmonary ...oxygen uptake kinetics (τV̇O2). To test whether this relationship is causal, we assessed the impact of hyperoxia on τV̇O2 and critical power during supine cycle exercise.
What is the main finding and its importance?
The results demonstrate that hyperoxia increased muscle oxygenation, reduced τV̇O2 (i.e. sped up the oxygen uptake kinetics) and, subsequently, increased critical power when compared with normoxia. These results therefore suggest that τV̇O2 is a determinant of the upper limit for steady‐state exercise, i.e. critical power.
The present study determined the impact of hyperoxia on the phase II time constant of pulmonary oxygen uptake kinetics (τV̇O2) and critical power (CP) during supine cycle exercise. Eight healthy men completed an incremental test to determine maximal oxygen uptake and the gas exchange threshold. Eight separate visits followed, whereby CP, τV̇O2 and absolute concentrations of oxyhaemoglobin (HbO2; via near‐infrared spectroscopy) were determined via four constant‐power tests to exhaustion, each repeated once in normoxia and once in hyperoxia (fraction of inspired O2 = 0.5). A 6 min bout of moderate‐intensity exercise (70% of gas exchange threshold) was also undertaken before each severe‐intensity bout, in both conditions. Critical power was greater (hyperoxia, 148 ± 29 W versus normoxia, 134 ± 27 W; P = 0.006) and the τV̇O2 reduced (hyperoxia, 33 ± 12 s versus normoxia, 52 ± 22 s, P = 0.007) during severe exercise in hyperoxia when compared with normoxia. Furthermore, HbO2 was enhanced in hyperoxia compared with normoxia (hyperoxia, 67 ± 10 μm versus normoxia, 63 ± 11 μm; P = 0.020). The τV̇O2 was significantly related to CP in hyperoxia (R2 = 0.89, P < 0.001), but no relationship was observed in normoxia (r = 0.07, P = 0.68). Muscle oxygenation was increased, τV̇O2 reduced and CP increased in hyperoxia compared with normoxia, suggesting that τV̇O2 is an independent determinant of CP. The finding that τV̇O2 was related to CP in hyperoxia but not normoxia also supports this notion.
Introduction
Cocoa flavanols (CF) may exert health benefits through their potent vasodilatory effects, which are perpetuated by elevations in nitric oxide (NO) bioavailability. These vasodilatory ...effects may contribute to improved delivery of blood and oxygen (O
2
) to exercising muscle.
Purpose
Therefore, the objective of this study was to examine how CF supplementation impacts pulmonary O
2
uptake (
V
˙
O
2
) kinetics and exercise tolerance in sedentary middle-aged adults.
Methods
We employed a double-blind cross-over, placebo-controlled design whereby 17 participants (11 male, 6 female; mean ± SD, 45 ± 6 years) randomly received either 7 days of daily CF (400 mg) or placebo (PL) supplementation. On day 7, participants completed a series of ‘step’ moderate- and severe-intensity exercise tests for the determination of
V
˙
O
2
kinetics.
Results
During moderate-intensity exercise, the time constant of the phase II
V
˙
O
2
kinetics (
τ
V
˙
O
2
) was decreased by 15% in CF as compared to PL (mean ± SD; PL 40 ± 12 s vs. CF 34 ± 9 s,
P
= 0.019), with no differences in the amplitude of
V
˙
O
2
(
A
V
˙
O
2
; PL 0.77 ± 0.32 l min
−1
vs. CF 0.79 ± 0.34 l min
−1
,
P
= 0.263). However, during severe-intensity exercise,
τ
V
˙
O
2
, the amplitude of the slow component (
SC
V
˙
O
2
) and exercise tolerance (PL 435 ± 58 s vs. CF 424 ± 47 s,
P
= 0.480) were unchanged between conditions.
Conclusion
Our data show that acute CF supplementation enhanced
V
˙
O
2
kinetics during moderate-, but not severe-intensity exercise in middle-aged participants. These novel effects of CFs, in this demographic, may contribute to improved tolerance of moderate-activity physical activities, which appear commonly present in daily life.
Trial registration
Registered under ClinicalTrials.gov Identifier no. NCT04370353, 30/04/20 retrospectively registered
Critical power (CP) is a fundamental parameter defining high-intensity exercise tolerance; however, its physiological determinants are incompletely understood. The present study determined the impact ...of hyperoxia on CP, the time constant of phase II pulmonary oxygen uptake kinetics (τV˙O2), and muscle oxygenation (assessed by near-infrared spectroscopy) in nine healthy men performing upright cycle ergometry.
Critical power was determined in normoxia and hyperoxia (fraction of inspired O2 = 0.5) via four severe-intensity constant load exercise tests to exhaustion on a cycle ergometer, repeated once in each condition. During each test, τV˙O2 and the time constant of muscle deoxyhemoglobin kinetics (τHHb), alongside absolute concentrations of muscle oxyhemoglobin (HbO2), were determined.
Critical power was greater (hyperoxia, 216 ± 30 W vs normoxia, 197 ± 29 W; P < 0.001), whereas W' was reduced (hyperoxia, 15.4 ± 5.2 kJ; normoxia, 17.5 ± 4.3 W; P = 0.037) in hyperoxia compared with normoxia. τV˙O2 (hyperoxia, 35 ± 12 s vs normoxia, 33 ± 10 s; P = 0.33) and τHHb (hyperoxia, 11 ± 5 s vs normoxia, 14 ± 5 s; P = 0.65) were unchanged between conditions, whereas HbO2 during exercise was greater in hyperoxia compared with normoxia (hyperoxia, 73 ± 20 vs normoxia, 66 ± 15 μM; P < 0.001).
This study provides novel insights into the physiological determinants of CP and by extension, exercise tolerance. Microvascular oxygenation and CP were improved during exercise in hyperoxia compared with normoxia. Importantly, the improved microvascular oxygenation afforded by hyperoxia did not alter τV˙O2, suggesting that microvascular O2 availability is an independent determinant of the upper limit for steady-state exercise, that is, CP.
We have previously demonstrated that the phase II time constant of pulmonary oxygen uptake kinetics (τv˙o2) is an independent determinant of critical power (CP) when O2 availability is not limiting, ...that is, during upright cycle exercise in young, healthy individuals. Whether this causative relationship remains when O2 availability is impaired remains unknown. During supine exercise, which causes an O2 availability limitation during the exercise transition, we therefore determined the impact of a raised baseline work rate on τv˙o2 and CP. CP, τv˙o2, and muscle oxygenation status (the latter via near‐infrared spectroscopy) were determined via four severe‐intensity constant‐power exercise tests completed in two conditions: (1) with exercise initiated from an unloaded cycling baseline (U→S), and (2) with exercise initiated from a moderate‐intensity baseline work rate of 90% of the gas exchange threshold (M→S). In M→S, critical power was lower (U→S = 146 ± 39 W vs. M→S = 132 ± 33 W, P = 0.023) and τv˙o2 was greater (U→S = 45 ± 16 sec, vs. M→S = 69 ± 129 sec, P = 0.001) when compared to U→S. There was no difference in tissue oxyhemoglobin concentration (HbO2 + MbO2) at baseline or during exercise. The concomitant increase in τv˙o2 and reduction in CP during M→S compared to U→S shows for the first time that τv˙o2 is an independent determinant of CP in conditions where O2 availability is limiting.
We have previously shown that oxygen uptake kinetics are a determinant of critical power in the upright position, where oxygen availability is not limiting. The present data show that in the supine position, which causes an oxygen availability limitation, slowing oxygen uptake kinetics via work‐to‐work exercise resulted in a reduction in critical power. Hence, this study suggests that oxygen uptake kinetics are an important determinant of critical power, regardless of the sufficiency of oxygen availability.
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