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The functional threshold power (FTP) field test is appealing for junior cyclists, but it was never investigated in this age category, and even in adults, there are few data on FTP collected in field conditions. Nine male junior road cyclists (16.9 ± 0.8 years) performed laboratory determination of maximal aerobic power (MAP), 4-mM lactate threshold (P4mM), critical power (CP), and the curvature constant (W′), plus a field determination of FTP as 95% of the average power output during a 20-minute time trial in an uphill road. The level of significance was set at p < 0.05. Outdoor FTP (269 ± 34 W) was significantly higher than CP (236 ± 24 W) and P4mM (233 ± 23 W). The VO2peak of the field FTP test (66.9 ± 4.4 ml·kg−1·min−1) was significantly higher than the VO2peak assessed in the laboratory (62.7 ± 3.7 ml·kg−1·min−1). Functional threshold power was correlated, in descending order, with MAP (r = 0.95), P4mM (r = 0.94), outdoor and indoor VO2 peak (r = 0.93 and 0.93, respectively), CP (r = 0.84), and W′ (r = 0.66). It follows that in junior road cyclists, the FTP field test was feasible and related primarily to aerobic endurance parameters and secondarily, but notably, to W′. However, the FTP field test significantly exceeded all laboratory performance tests. When translating laboratory results to outdoor uphill conditions, coaches and sport scientists should consider this discrepancy, which may be particularly enhanced in this cycling age category.

Purpose: Cardiovascular responses during resting apnoea include three phases: (1) a dynamic phase of rapid changes, lasting at most 30s; (2) a subsequent steady phase; and (3) a further dynamic phase, with a continuous decrease in heart rate (HR) and an increase in blood pressure. The interpretation was that the end of the steady phase corresponds to the physiological apnoea breaking point. This being so, during exercise apnoeas, the steady phase would be shorter, and the rate of cardiovascular changes in the subsequent unsteady phase would be faster than at rest. Methods: To test these hypotheses, we measured beat-by-beat systolic (SBP), diastolic, and mean blood pressures (MBP), HR, and stroke volume (SV) in six divers during dry resting (duration 239.4±51.6s) and exercise (30W on cycle ergometer, duration 88.2±20.9s) maximal apnoeas, and we computed cardiac output ( $$\dot{Q}$$ Q ˙ ) and total peripheral resistance (TPR). Results: Compared to control, at the beginning of resting (R1) and exercising (E1) apnoeas, SBP and MBP decreased and HR increased. SV and $$\dot{Q}$$ Q ˙ fell, so that TPR remained unchanged. At rest, HR, SV, $$\dot{Q}$$ Q ˙ , and SBP were stable during the subsequent phase; this steady phase was missing in exercise apnoeas. Subsequently, at rest (R3) and at exercise (E2), HR decreased and SBP increased continuously. SV returned to control values. Since $$\dot{Q}$$ Q ˙ remained unchanged, TPR grew. Conclusions: The lack of steady phase during exercise apnoeas suggests that the conditions determining R3 were already attained at the end of E1. This being so, E2 would correspond to R3.

Background: Post-traumatic cerebral infarction (PTCI) is common after traumatic brain injury (TBI). It is unclear what the occurrence of a PTCI is, how it impacts the long-term outcome, and whether it adds incremental prognostic value to established outcome predictors. Methods: This was a prospective multicenter cohort study of moderate and severe TBI patients. The primary objective was to evaluate if PTCI was an independent risk factor for the 6-month outcome assessed with the Glasgow Outcome Scale (GOS). We also assessed the PTCI occurrence and if it adds incremental value to the International Mission for Prognosis and Clinical Trial design in TBI (IMPACT) core and extended models. Results: We enrolled 143 patients, of whom 47 (32.9%) developed a PTCI. In the multiple ordered logistic regression, PTCI was retained in both the core and extended IMPACT models as an independent predictor of the GOS. The predictive performances increased significantly when PTCI was added to the IMPACT core model (AUC = 0.73, 95% C.I. 0.66-0.82; increased to AUC = 0.79, 95% CI 0.71-0.83, p = 0.0007) and extended model (AUC = 0.74, 95% C.I. 0.65-0.81 increased to AUC = 0.80, 95% C.I. 0.69-0.85; p = 0.00008). Patients with PTCI showed higher ICU mortality and 6-month mortality, whereas hospital mortality did not differ between the two groups. Conclusions: PTCI is a common complication in patients suffering from a moderate or severe TBI and is an independent risk factor for long-term disability. The addition of PTCI to the IMPACT core and extended predictive models significantly increased their performance in predicting the GOS.

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.

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.