No abstract

This study examined the effect of pedal cadence on the heterogeneity of muscle deoxygenation during exercise of moderate intensity. Twelve healthy subjects performed 6 min of cycling at 40 and 100 r · min(-1) at 80% of the workload corresponding to the gas exchange threshold. Gas exchanges were measured breath by breath during each exercise. Muscle deoxygenation (HHb, i.e., O2 extraction) was monitored continuously by near-infrared spectroscopy at eight sites on the vastus lateralis. The heterogeneity of HHb was assessed using the relative dispersion of the signal measured at the eight sites (i.e., 100 × standard deviation/mean). HHb was not altered by the pedal cadence, whereas pulmonary V̇O2 was higher at 100 r · min(-1) than at 40 r · min(-1) (p < 0.001). The relative dispersion of HHb was significantly higher at 100 r · min(-1) than at 40 r · min(-1) (p < 0.001). These results indicate that pedal cadence has no effect on O2 extraction but that an elevated cadence would increase muscle V̇O2, suggesting an increase in muscle blood flow. Elevated cadence also induced greater heterogeneity of the muscle's V̇O2/Q̇O2 delivery ratio, suggesting a change in the adequacy between O2 demand and O2 delivery in some regions of active muscle.

This study analyzed baroreflex sensitivity, heart rate and systolic blood pressure variabilities during an oral 1 week administration of prednisone. This study examined the hypothesis that prednisone might change both systolic blood pressure level and baroreflex sensitivity. Twelve physically active male subjects participated to a double-blind, randomized cross-over study consisting of two 1-week periods of treatment separated by a 4-week drug-free washout period: placebo (PLA) or prednisone (PRED). Trials were performed by each subject four times on the second (D2) and seventh (D7) day of each treatment period. ECG and blood pressure were continuously recorded to compute heart rate variability, systolic blood pressure variability and baroreflex sensitivity components with the smoothed pseudo Wigner Ville distribution and baroreflex analysis. Following D2 prednisone treatment, both HR (PLA: 60.8 ± 10.5 vs. PRED: 65.8 ± 9.1 beats min−1, p = 0.008) and low frequency component of systolic blood pressure variability (D2: 3.09 ± 0.19 vs. D7: 2.34 ± 0.19, p < 0.041) increased whereas other components did not change. Over 7 days of treatment, LF-SBP amplitude increased (D2: 2.71 ± 0.89 vs. D7: 3.87 ± 0.6 mmHg, p = 0.037). A slight increase in both HR and LF-SBPV were observed suggesting a potential sympathetic cardiovascular stimulus. Although we found a significant effect of the 1-week prednisone treatment on heart rate and low frequency power of systolic blood pressure variability, we reported neither an increase in the systolic blood pressure level nor a decrease in the baroreflex sensitivity. Therefore, the fragility of our results cannot support a deleterious effect of 1-week administration of prednisone on the autonomic cardiovascular control which might be involved in cardiovascular diseases.

The aim was to assess the cardiac, arterial oxygen saturation, lactate, hormonal and Borg rating of perceived exertion (RPE) responses to acute apnea in relation to apnea capacity in 18 middle-aged triathletes. Subjects were monitored while swimming two 50-m freestyle exercise trials with fins at maximal speed: with normal frequency breathing (NB) and with complete apnea (Ap); the latter was used to assess apnea capacity. The subjects with significant alteration in swimming performance inducing a time increase greater than 2.5% during Ap vs. NB were put in the group: bad apnea capacity (Bad Ap); the others, who showed no significant alteration in performance, were put in the group: Good Ap. Under apnea, both groups showed a decrease in arterial oxygen saturation (p<0.05). In Ap conditions, only Bad Ap had a significant lower maximal heart rate vs. NB (p<0.05), with lower blood lactate (p<0.05) and arm stroke frequency (p<0.01). No change in saliva hormonal concentrations was found during the experiment for both groups, whereas RPE responses were increased in the Good Ap group under Ap vs. NB conditions. In conclusion, a good apnea capacity seems to be associated with lower cardiovascular and metabolic apnea alterations in middle-aged recreationally-trained triathletes.

The aim of this study was to determine the influence of swim intensity on acute responses to dynamic apnoea. 9 swimmers performed one 50 m front crawl trial in four different conditions: at 400 m velocity (V) with normal breathing (NB), at V in complete apnoea (Ap), at maximal velocity (V) with NB and at V in Ap. Peak heart rate (HR), blood lactate concentration after exercise (Lac) and Borg rating of perceived exertion (RPE) were measured. Arterial oxygen saturation (SpO) was monitored with a pulse oximeter at forehead level during and after exercise. In Ap, swimming at V induced a significantly lower HR and Lac than swimming at V whilst RPE and the kinetics of SpO were not different at V and at V. The minimal value of SpO in Ap was reached 10 to 11 s after the end of V and V (81.7 ± 10.1% and 84.4 ± 10.6%, respectively). Swimming a 50 m front crawl in Ap resulted in a large decrease in SpO which occurred only after the cessation of exercise. The higher duration of apnoea during submaximal exercise could explain why SpO and RPE reached the same values as for maximal exercise.​.

These results indicate that high aerobic fitness (1) allows for better regulation between [Formula: see text]O2M and VO2M following the change in pedaling cadence, and (2) is the most important factor in the relationship between pedaling cadence and performance.

Significant alteration in hypothalamic-pituitary-adrenal function has been demonstrated in patients after short-term glucocorticoid therapy, but its impact on the circadian rhythm of steroid hormones has never been investigated. This study examined the effects of short-term prednisone administration on the diurnal patterns of dehydroepiandrosterone (DHEA) and testosterone. Saliva samples were collected from 11 healthy, physically active, male volunteers for DHEA and testosterone analysis, as follows: every 4 h from 0800 to 2000 h on 2 control days without medication, and after 1 week of oral therapeutic prednisone treatment (60 mg daily) (days 0-3). Overall, a diurnal decline in the two steroid hormones was observed on the control days. After short-term glucocorticoid administration, DHEA concentrations were significantly decreased with a complete disappearance of the DHEA diurnal pattern, which lasted 2 days post-treatment. No glucocorticoid effect was observed for testosterone. The results indicate that short-term prednisone treatment affects the circadian pattern of saliva DHEA but not testosterone in healthy active volunteers. Further studies are necessary to determine whether this alteration in DHEA circadian pattern has clinical consequences in patients with chronic glucocorticoid therapy.

Glucocorticoids are among the most commonly used drugs. They are widely administered for acute and chronic musculoskeletal pain, as well as for several other pain syndromes, although their therapeutic use is sometimes diverted for doping purposes. Their time-course effects on hormonal and inflammatory responses nevertheless remain poorly understood, both at rest and during exercise. We therefore studied the alterations induced by 1 week of prednisone treatment (60 mg daily) in recreationally trained male athletes after 2 days (i. e., acute) and 7 days (i. e., short-term). Hormonal (i. e., DHEA, DHEA-S, aldosterone, and testosterone) and pro- and anti-inflammatory markers (i. e., IL-6, IL-10, and IL-1β) were investigated at rest and after resistance exercise. A significant decrease in DHEA and DHEA-S (p<0.01) without change in the DHEA/DHEA-S ratio, aldosterone, or testosterone was demonstrated after acute prednisone intake. A significant increment in IL-10 and a significant decrement in IL-6 (p<0.05) were also observed with prednisone both at rest and during exercise, without significant change in IL-1β. Continued prednisone treatment led to another significant decrease in both DHEA and DHEA-S (p<0.05), whereas no change in the inflammatory markers was observed between days 2 and 7. Our data demonstrate that the anti-inflammatory effects of prednisone were maximal and stable from the beginning of treatment, both in rest and exercise conditions. However, hormonal concentrations continued to decline during short-term intake. Further studies are needed to determine the effects of hormonal time-course alterations with longer glucocorticoid treatment and the clinical consequences.