1,721,055 research outputs found
Effect of incomplete recovery on V’O2-on-kinetics during moderate-intensity exercise transitions in healthy humans
No full textV’O2 kinetics are slowed when exercise transitions begin from an elevated work and/or metabolic rate. Slower O2 provision, recruitment of fast fibres, reduced muscle energy status and phosphocreatine concentration ([PCr]) have been the proposed mechanisms. Incomplete recovery is associated with an elevated baseline V’O2 and with a reduced [PCr]) have been the proposed mechanisms. Incomplete recovery is associated with an elevated baseline V’O2 and with a reduced [PCr, with little effect on recruitment and O2 delivery. PURPOSE: We tested the hypothesis that pre-transition metabolic rate and/or [PCr] set the time course of the adjustment of oxidative metabolism: the lower the recovery time, the slower the VO2 kinetics.
METHODS: In 7 young active males (24±2 yrs, 48±11 ml·kg-1·min-1), we measured breath by breath alveolar V’O2 kinetics during a sequence of 6 moderate intensity step transitions, each lasting 6 min. Pre-transition V’O2 and intramuscular [PCr] were manipulated by progressively reducing the recovery time, in random order, at 30 s, 60 s, 90 s, 120 s and 300 s. V’O2 data from the 6 repetitions of the same transition were combined and fitted with a monoexponential model (excluding the initial 20s of data) to calculate phase 2 time constant (τ2) of V’O2 kinetics. [PCr] changes, from a baseline value of 25 mmol·Kg-1 of muscle, were estimated based on oxygen deficit.
recovery time (s) baseline VO2
(ml·min-1) steady state VO2
(ml·min-1) baseline [PCr]
(mmol·kg-1) τ2
(s)
300 507±83 1943±136 23.6±2.3 21.4±7.3
120 580±95* 1970±129 26.2±3.5 19.6 ± 4.4
90 660±120* 1976±133 23.5±3.4 18.6 ± 4.9
60 892±134* 1981±136 19.7±4.5* 21.4 ± 5.5
30 1323±134* 1977±119 18.1±4.5* 28.7 ± 8.0*
* indicates a significant difference (repeated measures ANOVA) form complete recovery (i.e. 300s)
RESULTS: Steady state V’O2 was unaffected by recovery time. Pre-transition V’O2 decreased and [PCr] increased linearly with recovery time up to 120s (r2=0.91 and 0.98, respectively). τ2 linearly increased with baseline metabolic rate and decreased with baseline [PCr] (r2 = 0.77 and 0.63 respectively). CONCLUSION: Our data favor the hypothesis that baseline metabolic rate and [PCr] affect the time course of the adjustment of oxidative metabolism. A lower energy status and altered PCr splitting kinetics could be responsible for a slower activation of oxidative phosphorylation and in turn, slower the V’O2 kinetics
Effect of high-intensity-interval-training (HIT) on maximal aerobic power and ventilatory threshold in older adults
No full textWe tested if 8 weeks of HIT can induce a significant increase of V’O2max and of the V’O2
corresponding to gas exchange threshold (GET) and to respiratory compensation point (RCP)
in older men. To this aim, we measured in 12 healthy male volunteers (68.7±3.9 yy;
79.0±10.8 kg, 171.4±5.4 cm) V’O2max, GET and RCP before (PRE) and after (POST) 8 weeks
of HIT performed 3 times a week cycling 7 times for 2 minutes, interspersed with 2 minutes
of recovery, at about 85-90 % of V’O2max. GET was measured during an incremental test up to
the limit of individual tolerance. V’O2max was measured during a subsequent
constant–workload test performed at 105 % the maximal work-rate achieved on the ramp test.
Absolute and relative V’O2max significantly increased by 5.4 % (PRE: 2.34±0.32 l/min; POST:
2.48±0.29 l/min, p < 0.05, effect size (ES) = 0.7) and 11.7 % (PRE: 28.8±5.66 ml/min kg;
POST: 32.6±5.66 ml/min kg, p < 0.05, ES = 0.8), respectively. V’O2 at GET and RCP
increased by 7.2% (PRE: 17.0±2.86 ml/min kg; POST: 18.3±3.81 ml/min kg, p < 0.05, ES =
0.7) and 15.4 % (PRE: 22.8±3.75 ml/min kg; POST: 27.0±5.30 ml/min kg, p < 0.05, ES =
1.3), respectively. Moreover, RCP increased from 76.5 % of V’O2max to 82.9 % of V’O2max (p
<0.05, ES = 0.7). It is concluded that 8 weeks of HIT are able to induce significant increases
of V’O2max and of exercise resistance in older adults
Mitochondrial coupling in humans: assessment of the P/O2 ratio at the onset of calf exercise
No full textCoupling of oxidation to ATP synthesis (P/O2 ratio) is a critical step in the conversion of carbon substrates to fuel (ATP) for cellular activity. The ability to quantitatively assess mitochondrial coupling in vivo can be a valuable tool for basic research and clinical purposes. At the onset of a square wave moderate
exercise, the ratio between absolute amount of phosphocreatine
split and O2 deficit (corrected for the amount of O2 released from the body O2 stores and in the absence of lactate production), is the mirror image of the P/O2 ratio. To calculate this value, cardiac output Q'; whole bodyO2 uptake V'O2;O2 deficit O2def and high-energy phosphates concentration (by 31P-NMR spectroscopy) in the calf muscles were measured on nine healthy volunteers at rest and during moderate intensity plantar flexion exercise (3.44 ± 0.73 W per unit active muscle mass). _Q and _V O2 increased (from 4.68 ± 1.56 to 5.83 ± 1.59 l min–1 and from 0.28 ± 0.05 to 0.48 ± 0.09 l min–1, respectively), while phosphocreatine (PCr) concentration decreased significantly
(22 ± 6%) from rest to steady-state exercise. For each volunteer, ‘‘gross’’ O2def was corrected for the individual
changes in the venous blood O2 stores (representing 49.9 +- 9.5% of the gross O2def) yielding the ‘‘net’’ O2def. Resting PCr concentration was estimated from the appropriate spectroscopy data. The so calculated P/O2 ratio amounted on average to 4.24 ± 0.13 and was, in all nine subjects, very close to the literature values obtained directly on intact skeletal muscle. This unfolds the prospect of a non-invasive tool to quantitatively study mitochondrial coupling in vivo
Effects of localized and general fatigue on postural adjustments coupling during predictable external perturbations
Full text linkPurpose: The central nervous system (CNS) coordinates anticipatory (APA) and compensatory postural adjustments (CPA) to face both self-induced and external perturbations. Neuromuscular fatigue (NMF), whether localized or general, impairs the CNS's ability to maintain postural stability, but the differential effects of these fatigue types on the coupling between APA and CPA remain unclear. This study aimed to investigate how localized and general NMF influence the neuromuscular control of postural adjustments during predictable external perturbations. Methods: Fourteen participants were exposed to two exercise protocols: intermittent isometric exercise to induce localized NMF and prolonged upper body exercise at high cardiometabolic effort to induce general NMF. Exercise intensity was monitored by measuring cardiometabolic parameters during exercise and recovery. Postural adjustments were assessed before and after NMF (recovery period) using electromyography and kinematic analyses while participants were exposed to predictable perturbations. Results: Localized NMF led to decreased muscle activation and co-activation across both fatigued and non-fatigued muscles during APA, with persistent kinematic changes in lower limb joints. In contrast, general NMF induced short-lived increases in EMG activity and co-activation, reflecting a strategic CNS adaptation to maintain stability. Conclusions: The results suggest that localized NMF induces a more extensive and enduring impact on postural control mechanisms, likely due to altered proprioceptive feedback, whereas general NMF effects are more transient, aligning with the rapid recovery of cardiometabolic parameters. These findings highlight the CNS's role in differentially adapting postural strategies depending on the type of fatigue, with implications for understanding how fatigue impacts stability in dynamic environments
Can a short-term hiking training speed up V'O2-on kinetic in healthy sedentary women?
No full textWe tested the hypothesis that two weeks of training performed at moderate intensity can induce a significant acceleration of the V'02-on kinetics in adultsedentary women. To this aim, breath-by-breath oxygen uptake (V'02) was measured in 8 women (25 yy ± 7; 68 kg ± 11,165 cm ± 8) during: i) an incrementai ramp cycling test up to exhaustion and; ii) during three consecutive square wave tests performed at approximately 50 % of V'02max before and immediately after atraining program of daiiy trekking (6-3 hour/d) performed at near sea level and on irregular and undulating terrain.Absolute and relative V'02max values did not increase as a result of the hiking training. The time Constant of the primary phase (t2: PRE: 23.1 s ± 8; POST 16.4 ± 6) of V02 kinetics were significantly smaller after training (P < 0.05). Percent decrease of t2 was significantly and negativeìy correlated with absolute V'O atbaseline (r = 0.69, P < 0.05). It is concluded that two weeks of training performed at moderate intensity are able to induce a significant acceleration of the dynamicresponse of oxidative metabolism during exercise that is not paralleled by any increase of V'02max in healthy sedentary women. Moreover, the extent of the improvement is affected by the value of V'Omax at the baseline
Effect of recovery time on V ̇ O 2 -ON kinetics in humans at the onset of moderate-intensity cycling exercise
Full text linkPurpose: τ of the primary phase of ̇ VO 2A kinetics during square-wave, moderate-intensity exercise mirrors that of PCr splitting (τPCr). Pre-exercise [PCr] and the absolute variations of PCr (∆[PCr]) occurring during transient have been suggested to control τPCr and, in turn, to modulate ̇ VO 2A kinetics. In addition, ̇ VO 2A kinetics may be slower when exercise initiates from a raised metabolic level, i.e., from a less-favorable energetic state. We verified the hypothesis that: (i) pre-exercise [PCr], (ii) pre-exercise metabolic rate, or (iii) ∆[PCr] may affect the kinetics of muscular oxidative metabolism and, therefore, τ. Methods: To this aim, seven active males (23.0 yy ± 2.3; 1.76 m ± 0.06, ̇ VO 2 max : 3.32 L min −1 ± 0.67) performed three rep- etitions of series consisting of six 6-min step exercise transitions of identical workload interspersed with different times of recovery: 30, 60, 90, 120, 300 s. Results: Mono-exponential fitting was applied to breath-by-breath ̇ VO 2A , so that τ was determined. τ decays as a first-order exponential function of the time of recovery (τ = 109.5 × e(−t/14.0) + 18.9 r2 = 0.32) and linearly decreased as a function of the estimated pre-exercise [PCr] (τ = − 1.07 [PCr] + 44.9, r2 = 0.513, P < 0.01); it was unaffected by the estimated ∆[PCr]. Conclusions: Our results in vivo do not confirm the positive linear relationship between τ and pre-exercise [PCr] and ∆[PCr]. Instead, ̇ VO 2A kinetics seems to be influenced by the pre-exercise metabolic rate and the altered intramuscular energetic state
Postexercise cardiovascular hemodynamics assessment before and after a 30-minute standing still recovery
No full textBackground: Although postexercise syncope usually occurs shortly after physical exercise conclusion, athletes commonly reveal symptoms of postexercise hypotension several tens of minutes after exercise completion. Currently, no studies have investigated central hemodynamic regulation during posture changes occurring several tens of minutes after exercise compared to immediately after cessation. Methods: This study examined changes in mean arterial pressure (MAP), heart rate (HR), systemic vascular conductance (SVC), cardiac output, and stroke volume during two sets of tilt tests performed before vs. after a 30-minute standing still recovery, respectively. Tilt tests were performed after a short-lasting supramaximal test (WNG) and long-lasting maximal incremental test (INC) in 12 young endurance-trained individuals. Results: The key findings were that, regardless of the exercise type, the 30-minute recovery augmented (P<0.01) the increase in HR and the drop in SVC during the transition from supine to upright, although the MAP drop was similar (P=0.99) after vs. before recovery. INC led to greater increases (P<0.01) in HR and drops (P<0.01) in SVC compared to WNG during postural transitions both before and after the recovery. Conclusions: These findings suggest that, in a population that tolerates postexercise hypotension, MAP neural control is more challenged after a 30-minute standing still recovery than before, as evidenced by an augmented vasodilation capacity along with an increased HR buffering response during posture changes. Moreover, our data suggest that effective MAP control is resulting from an equally effective HR buffering response on MAP. Therefore, exercises that induce greater systemic vasodilation lead to greater HR buffering responses
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