Search

The aim of this study was to test the hypothesis that the maximal instantaneous muscular power of humans ( $$ \dot{w} $$ w ˙ p) is affected by the negative work performed immediately before the jump (w n), possibly due to the recoil of elastic strain energy stored in previously stretched series-elastic elements of the muscle-tendon complex. Twenty-seven Bantu subjects (age 25.1±4.3years, body mass 67.5±7.8kg) were investigated. The $$ \dot{w} $$ w ˙ p, the average power ( $$ \dot{w} $$ w ˙ a) and w n were determined during maximal vertical jumps off both feet on a force platform. Three jumping conditions were studied: squat jumps (SQ), countermovement jumps (CM), and jumps preceded by a free fall (FF) from a height of 0.3m above the platform surface. The w n was higher in CM than in SQ and in FF than in CM and SQ. The $$ \dot{w} $$ w ˙ p was 3.51±0.54kW in SQ and did not vary in CM and FF. The $$ \dot{w} $$ w ˙ a increased with increasing w n (1.70±0.30; 1.85±0.34; 1.99±0.31kW in SQ, CM and FF, respectively, p<0.05). The greater was the w n, the higher was the force at the start of the positive push phase, and thus the maximal force attained during the push phase. In conclusion, $$ \dot{w} $$ w ˙ p was independent of w n, whereas $$ \dot{w} $$ w ˙ a was affected, because a greater force was developed over a shorter time during the push. The independence of $$ \dot{w} $$ w ˙ p of w n leads to refutation of the tested hypothesis.

We hypothesised that vagal withdrawal and increased venous return interact in determining the rapid cardiac output (CO) response (phase I) at exercise onset. We used lower body negative pressure (LBNP) to increase blood distribution to the heart by muscle pump action and reduce resting vagal activity. We expected a larger increase in stroke volume (SV) and smaller for heart rate (HR) at progressively stronger LBNP levels, therefore CO response would remain unchanged. To this aim ten young, healthy males performed a 50 W exercise in supine position at 0 (Control), -15, -30 and -45 mmHg LBNP exposure. On single beat basis, we measured HR, SV, and CO. Oxygen uptake was measured breath-by-breath. Phase I response amplitudes were obtained applying an exponential model. LBNP increased SV response amplitude threefold from Control to -45 mmHg. HR response amplitude tended to decrease and prevented changes in CO response. The rapid response of CO explained that of oxygen uptake. The rapid SV kinetics at exercise onset is compatible with an increased venous return, whereas the vagal withdrawal conjecture cannot be dismissed for HR. The rapid CO response may indeed be the result of two independent yet parallel mechanisms, one acting on SV, the other on HR.

Introduction: Interpolation methods circumvent poor time resolution of breath-by-breath oxygen uptake ( $$\dot{V}{\text{O}}_{2}$$ V ˙ O 2 ) kinetics at exercise onset. We report an interpolation-free approach to the improvement of poor time resolution in the analysis of $$\dot{V}{\text{O}}_{2}$$ V ˙ O 2 kinetics. Methods: Noiseless and noisy (10% Gaussian noise) synthetic data were generated by Monte Carlo method from pre-selected parameters (Exact Parameters). Each data set comprised 10 ( $$\dot{V}{\text{O}}_{2}$$ V ˙ O 2 )-on transitions with noisy breath distribution within a physiological range. Transitions were superposed (no interpolation, None), then analysed by bi-exponential model. Fitted model parameters were compared with those from interpolation methods (average transition after Linear or Step 1-s interpolations), applied on the same data. Experimental data during cycling were also analysed. The 95% confidence interval around a line of parameters' equality was computed to analyse agreement between exact parameters and corresponding parameters of fitted functions. Results: The line of parameters' equality stayed within confidence intervals for noiseless synthetic parameters with None, unlike Step and Linear, indicating that None reproduced Exact Parameters. Noise addition reduced differences among pre-treatment procedures. Experimental data provided lower phase I time constants with None than with Step. Conclusion: In conclusion, None revealed better precision and accuracy than Step and Linear, especially when phenomena characterized by time constants of <30s are to be analysed. Therefore, we endorse the utilization of None to improve the quality of breath-by-breath $$\dot{V}{\text{O}}_{2}$$ V ˙ O 2 data during exercise transients, especially when a double exponential model is applied and phase I is accounted for.

If, as postulated, the end of the steady state phase (phi 2) of cardiovascular responses to apnoea corresponds to the physiological breaking point, then we may hypothesize that phi 2 should become visible if exercise apnoeas are performed in pure oxygen. We tested this hypothesis on 9 professional divers by means of continuous recording of blood pressure (BP), heart rate (f(H)), stroke volume (Q(S)), and arterial oxygen saturation (SpO(2)) during dry maximal exercising apnoeas in ambient air and in oxygen. Apnoeas lasted 45.0 +/- 16.9 s in air and 77.0 +/- 28.9 s in oxygen (p < 0.05). In air, no phi 2 was observed. Conversely, in oxygen, a phi 2 of 28 +/- 5 s duration appeared, during which systolic BP (185 +/- 29 mmHg), f(H) (93 +/- 16 bpm) and Q(S) (91 +/- 16 ml) remained stable. End-apnoea SpO(2) was 95.5 +/- 1.9% in air and 100% in oxygen. The results support the tested hypothesis.

Purpose: Morton (J Sport Sci 29:307-309, 2011) proposed a model of the peak power attained in ramp protocol ( $$\dot{w}_{\text{peak}}$$ w · peak ) that included critical power (CP) and anaerobic capacity as constants, and mean ramp slope (S) as variable. Our hypothesis is that $$\dot{w}_{\text{peak}}$$ w · peak depends only on S, so that Morton's model should be applicable in all types of ramps. The aim of this study was to test this hypothesis by validating Morton's model using stepwise ramp tests with invariant step increment and increasing step duration. Methods: Sixteen men performed six ramp tests with 25W increments. Step duration was: 15, 30, 60, 90, 120 and 180s. Maximal oxygen consumption ( $$\dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ V · O 2 max ) and $$\dot{w}_{\text{peak}}$$ w · peak were identified as the highest values reached during each test. An Åstrand-type test was also performed. We measured oxygen consumption and ventilatory variables, together with lactate and heart rate. Results: $$\dot{V}{\text{O}}_{2\hbox{max} }$$ V · O 2 max was the same in all tests; $$\dot{w}_{\text{peak}}$$ w · peak was significantly lower the longer the step duration, and all values differed from the maximal power of the Åstrand-type test ( $$\dot{w}_{\hbox{max} }$$ w · max ). Morton's model yielded an excellent fitting, with mean CP equal to 198.08±37.46W and anaerobic capacity equal to 16.82±5.69kJ. Conclusions: Morton's model is a good descriptor of the mechanics of ramp tests. Further developments of Morton's model demonstrated that, whereas $$\dot{w}_{\text{peak}}$$ w · peak is a protocol-dependent variable, the difference between $$\dot{w}_{\hbox{max} }$$ w · max and CP is a constant, so that their values do not depend on the protocol applied

At exercise steady state, the lower the arterial oxygen saturation (SaO2), the lower the O2 return $$(\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2}).$$ A linear relationship between these variables was demonstrated. Our conjecture is that this relationship describes a condition of predominant sympathetic activation, from which it is hypothesized that selective β1-adrenergic blockade (BB) would reduce O2 delivery $$(\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2} )$$ and $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} .$$ To test this hypothesis, we studied the effects of BB on $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2}$$ and $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} $$ in exercising humans in normoxia and hypoxia. O2 consumption $$(\ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{2} ),$$ cardiac output $$(\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}, CO_{2}\; \hbox{rebreathing}),$$ heart rate, SaO2 and haemoglobin concentration were measured on six subjects (age 25.5±2.4years, mass 78.1±9.0kg) in normoxia and hypoxia (inspired O2 fraction of 0.11) at rest and steady-state exercises of 50, 100, and 150W without (C) and with BB with metoprolol. Arterial O2 concentration (CaO2), $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2},$$ and $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}\bar{{\text{v}}} {\text{O}}_{2} $$ were then computed. Heart rate, higher in hypoxia than in normoxia, decreased with BB. At each $$\ifmmode\expandafter\dot\else\expandafter\.\fi{V}{\text{O}}_{2} ,$$ $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}$$ was higher in hypoxia than in normoxia. With BB, it decreased during intense exercise in normoxia, at rest, and during light exercise in hypoxia. SaO2 and CaO2 were unaffected by BB. The $$\ifmmode\expandafter\dot\else\expandafter\.\fi{Q}{\text{aO}}_{2} $$

On ten top-level Kenyan marathon runners (KA) plus nine European controls (EC, equivalent to KA), we measured maximal oxygen consumption ( $$ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $$ ) and the energy cost of running (C r) on track during training camps at moderate altitude, to better understand the KA dominance in the marathon. At each incremental running speed, steady-state oxygen consumption ( $$ \dot{V}{\text{O}}_{ 2} $$ ) was measured by telemetric metabolic cart, and lactate by electro-enzymatic method. The speed requiring $$ \dot{V}{\text{O}}_{ 2} = \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $$ provided the maximal aerobic velocity (v max). The energy cost of running was calculated by dividing net $$ \dot{V}{\text{O}}_{ 2} $$ by the corresponding speed. The speed at lactate threshold (v ΘAN) was computed from individual Lâb versus speed curves. The sustainable $$ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $$ fraction (F d) at v ΘAN (F ΘAN) was computed dividing v ΘAN by v max. The F d for the marathon (F mar) was determined as F mar=0.92 F ΘAN. Overall, $$ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $$ (64.9±5.8 vs. 63.9±3.7mlkg−1min−1), v max (5.55±0.30 vs. 5.41±0.29ms−1) and C r (3.64±0.28 vs. 3.63±0.31Jkg−1m−1) resulted the same in KA as in EC. In both groups, C r increased linearly with the square of speed. F ΘAN was 0.896±0.054 in KA and 0.909±0.068 in EC; F mar was 0.825±0.050 in KA and 0.836±0.062 in EC (NS). Accounting for altitude, running speed predictions from present data are close to actual running performances, if F ΘAN instead of F mar is taken as index of F d. In conclusion, both KA and EC did not have a very high $$ \dot{V}{\text{O}}_{{ 2 {\text{max}}}} $$ , but had extremely high F d, and low C r, equal between them. The dominance of KA over EC cannot be explained on energetic grounds

The aim of this study was to test the hypothesis that the maximal instantaneous muscular power of humans ( $$ \dot{w} $$ w ˙ p) is affected by the negative work performed immediately before the jump (w n), possibly due to the recoil of elastic strain energy stored in previously stretched series-elastic elements of the muscle-tendon complex. Twenty-seven Bantu subjects (age 25.1±4.3years, body mass 67.5±7.8kg) were investigated. The $$ \dot{w} $$ w ˙ p, the average power ( $$ \dot{w} $$ w ˙ a) and w n were determined during maximal vertical jumps off both feet on a force platform. Three jumping conditions were studied: squat jumps (SQ), countermovement jumps (CM), and jumps preceded by a free fall (FF) from a height of 0.3m above the platform surface. The w n was higher in CM than in SQ and in FF than in CM and SQ. The $$ \dot{w} $$ w ˙ p was 3.51±0.54kW in SQ and did not vary in CM and FF. The $$ \dot{w} $$ w ˙ a increased with increasing w n (1.70±0.30; 1.85±0.34; 1.99±0.31kW in SQ, CM and FF, respectively, p<0.05). The greater was the w n, the higher was the force at the start of the positive push phase, and thus the maximal force attained during the push phase. In conclusion, $$ \dot{w} $$ w ˙ p was independent of w n, whereas $$ \dot{w} $$ w ˙ a was affected, because a greater force was developed over a shorter time during the push. The independence of $$ \dot{w} $$ w ˙ p of w n leads to refutation of the tested hypothesis.

Introduction: Interpolation methods circumvent poor time resolution of breath-by-breath oxygen uptake ( $$\dot{V}{\text{O}}_{2}$$ V ˙ O 2 ) kinetics at exercise onset. We report an interpolation-free approach to the improvement of poor time resolution in the analysis of $$\dot{V}{\text{O}}_{2}$$ V ˙ O 2 kinetics. Methods: Noiseless and noisy (10% Gaussian noise) synthetic data were generated by Monte Carlo method from pre-selected parameters (Exact Parameters). Each data set comprised 10 ( $$\dot{V}{\text{O}}_{2}$$ V ˙ O 2 )-on transitions with noisy breath distribution within a physiological range. Transitions were superposed (no interpolation, None), then analysed by bi-exponential model. Fitted model parameters were compared with those from interpolation methods (average transition after Linear or Step 1-s interpolations), applied on the same data. Experimental data during cycling were also analysed. The 95% confidence interval around a line of parameters' equality was computed to analyse agreement between exact parameters and corresponding parameters of fitted functions. Results: The line of parameters' equality stayed within confidence intervals for noiseless synthetic parameters with None, unlike Step and Linear, indicating that None reproduced Exact Parameters. Noise addition reduced differences among pre-treatment procedures. Experimental data provided lower phase I time constants with None than with Step. Conclusion: In conclusion, None revealed better precision and accuracy than Step and Linear, especially when phenomena characterized by time constants of <30s are to be analysed. Therefore, we endorse the utilization of None to improve the quality of breath-by-breath $$\dot{V}{\text{O}}_{2}$$ V ˙ O 2 data during exercise transients, especially when a double exponential model is applied and phase I is accounted for.

Purpose: Morton (J Sport Sci 29:307-309, 2011) proposed a model of the peak power attained in ramp protocol ( $$\dot{w}_{\text{peak}}$$ w · peak ) that included critical power (CP) and anaerobic capacity as constants, and mean ramp slope (S) as variable. Our hypothesis is that $$\dot{w}_{\text{peak}}$$ w · peak depends only on S, so that Morton's model should be applicable in all types of ramps. The aim of this study was to test this hypothesis by validating Morton's model using stepwise ramp tests with invariant step increment and increasing step duration. Methods: Sixteen men performed six ramp tests with 25W increments. Step duration was: 15, 30, 60, 90, 120 and 180s. Maximal oxygen consumption ( $$\dot{V}{\text{O}}_{{ 2 {\text{max}}}}$$ V · O 2 max ) and $$\dot{w}_{\text{peak}}$$ w · peak were identified as the highest values reached during each test. An Åstrand-type test was also performed. We measured oxygen consumption and ventilatory variables, together with lactate and heart rate. Results: $$\dot{V}{\text{O}}_{2\hbox{max} }$$ V · O 2 max was the same in all tests; $$\dot{w}_{\text{peak}}$$ w · peak was significantly lower the longer the step duration, and all values differed from the maximal power of the Åstrand-type test ( $$\dot{w}_{\hbox{max} }$$ w · max ). Morton's model yielded an excellent fitting, with mean CP equal to 198.08±37.46W and anaerobic capacity equal to 16.82±5.69kJ. Conclusions: Morton's model is a good descriptor of the mechanics of ramp tests. Further developments of Morton's model demonstrated that, whereas $$\dot{w}_{\text{peak}}$$ w · peak is a protocol-dependent variable, the difference between $$\dot{w}_{\hbox{max} }$$ w · max and CP is a constant, so that their values do not depend on the protocol applied