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Visual performance is impaired when the ocular blood flow decreases, indicating that ocular blood flow plays a role in maintaining visual performance during exercise. We examined the ocular blood flow response to incremental cycling exercise to test the hypothesis that ocular blood flow is relatively stable during dynamic exercise because of its autoregulatory nature. The blood flow in the inferior and superior temporal retinal arterioles (ITRA and STRA, respectively) and retinal and choroidal vessels (RCV), mean arterial pressure, and heart rate (HR) were measured at rest and during leg cycling in nine young and healthy subjects (26 ± 5 years, mean ± SD). Ocular blood flow was measured by laser speckle flowmetry. The exercise intensity was incremented by 30 W every 3 min until the subject was unable to maintain a position appropriate for measuring ocular blood flow. Blood flow data obtained during cycling exercise were categorized based on HR as follows: <100, 100-120, and >120 bpm. Blood flow in the RCV increased with the exercise intensity: by 16 ± 8, 32 ± 13, and 40 ± 19% from baseline, respectively. However, blood flow and vascular conductance in the ITRA and STRA did not change significantly with exercise. These findings demonstrate for the first time that ocular blood flow increases in the retina and choroid, but not in the arterioles, with increasing exercise intensity during dynamic exercise. [ABSTRACT FROM AUTHOR]

This review focuses on the characteristics of heat-loss responses during exercise with respect to non-thermal factors. In addition, the effects of physical training on non-thermal heat-loss responses are discussed. When a subject is already sweating the sweating rate increases at the onset of dynamic exercise without changes in core temperature, while cutaneous vascular conductance (skin blood flow) is temporarily decreased. Although exercise per se does not affect the threshold for the onset of sweating, it is possible that an increase in exercise intensity induces a higher sensitivity of the sweating response. Exercise increases the threshold for cutaneous vasodilation, and at higher exercise intensities, the sensitivity of the skin-blood-flow response decreases. Facilitation of the sweating response with increased exercise intensity may be due to central command, peripheral reflexes in the exercising muscle, and mental stimuli, whereas the attenuation of skin-blood-flow responses with decreased cutaneous vasodilation is related to many non-thermal factors. Most non-thermal factors have negative effects on magnitude of cutaneous vasodilation; however, several of these factors have positive effects on the sweating response. Moreover, thermal and non-thermal factors interact in controlling heat-loss responses, with non-thermal factors having a greater impact until core temperature elevations become significant, after which core temperature primarily would control heat loss. Finally, as with thermally induced sweating responses, physical training seems to also affect sweating responses governed by non-thermal factors. [ABSTRACT FROM AUTHOR]

The purpose of the study was to examine the acute effect of a strength training session on brain-derived neurotrophic factor and insulin-like growth factor 1. Furthermore, the influence of a 10-week strength training program on brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF-1) resting levels and memory performance was studied. Fifteen untrained subjects followed a strength training program for 10 weeks. Eight control subjects remained physically inactive. To study the influence of an acute strength training session, blood samples were taken before and after the sixth and 30th sessions. Training effects were evaluated by taking blood samples at rest before and following the training program. Short- and mid-term memories were assessed using the digit span and a recall of images test. BDNF, IGF-1 and its binding protein (IGFBP-3) were measured in serum samples. Data were analyzed (p < 0.05) using a mixed design ANOVA model, Duncan's multiple range post hoc tests, and Pearson's correlation. A single strength training session did not influence BDNF and IGF-1 concentrations. No effect of the strength training period on BDNF, IGF-1, and IGFBP-3 was found. No correlation was found between peripheral BDNF and IGF-1. Short-term memory improved in both the experimental and control groups, but no difference between groups was present. Mid-term memory did not improve following the 10 weeks of training. A period of strength training in sedentary subjects does not significantly change the growth factors or memory function compared to a control group. Also, BDNF and IGF-1 are not acutely influenced by a training session. Further research should focus on the beneficial role of physical exercise in neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

We used unilateral plantar-flexor muscles fatigue to assess the capacity of the central nervous system to adapt quiet two-legged stance control to a unilateral ankle neuromuscular perturbation. Eighteen young healthy adults stood barefoot with their eyes closed and were asked to sway as little as possible. The Experimental group (n = 9) executed this postural task in two conditions, before (pre-test) and following the completion of a fatiguing exercise designed to induce a muscular fatigue in the plantar-flexor muscles of their dominant leg (post-test). For the Control group (n = 9), this fatiguing exercise was replaced with a standing rest period corresponding to the fatiguing exercise. Results of the Experimental group showed no significant difference between the weightbearing index measured in the pre-test condition and that observed in the post-test condition. Results further revealed that unilateral plantar-flexor muscles fatigue yielded different effects on the centre of foot pressure (CoP) displacements under the non-fatigued leg and under the fatigued leg: a wider surface area of the CoP displacements was observed under the non-fatigued than under the fatigued leg, and a higher mean speed of the CoP displacements was observed under the non-fatigued leg only in the post-test relative to the pre-test condition. These findings evidenced that the contribution of each leg to the control of quiet two-legged stance is modified as a result of muscle fatigue of unilateral plantar-flexor muscles. The greater contribution of the non-fatigued leg could be viewed as a fatigue-induced adaptive change in the control of quiet two-legged stance in response to an alteration of the unilateral ankle neuromuscular function induced by unilateral plantar-flexor muscles fatigue. [ABSTRACT FROM AUTHOR]

We compared two methods to determine IL-6 at rest and following exercise. On two occasions, plasma IL-6 was determined in 10 men and 13 women before and immediately following 90 min of cycling at 65% V(O)(2max) using a cytometric bead array (CBA) and an ELISA. The CBA detected IL-6 in 63% of pre-exercise samples and 84% of post-exercise samples; the ELISA detected IL-6 in all samples. In samples with detectable IL-6, resting values were comparable between the CBA and ELISA (2.3 +/- 1.0 and 2.4 +/- 1.2 pg/mL, respectively; p = 0.99); the IL-6 response to exercise was underestimated (p = 0.0003) by the CBA by ~45%, compared with the ELISA. CBA- and ELISA-determined IL-6 values were moderately correlated (r = 0.66, p < 0.0001), but exhibited poor agreement (mean bias +/- 1SD = -1.4 +/- 2.1 pg/mL). The CBA provided concordant IL-6 concentrations at rest, when detected, but underestimated exercise-induced increases in IL-6 versus the ELISA method. [ABSTRACT FROM AUTHOR]

Four elderly women (78 +/- 4.3 years) were resistance trained (RT) for one year and needle biopsies of the vastus lateralis muscle were taken pre- and post-RT. A training intensity of 60% one-repetition maximum (1RM) was adopted for the entire duration of the study. Following RT, significant gain in isometric force of the quadriceps muscles was observed and MHC isoform distribution of vastus lateralis muscle showed a very significant shift from MHC-1 and MHC-2X towards MHC-2A, i.e. a bi-directional shift. A large population (n = 310) of individual skinned muscle fibres were dissected from biopsy samples and used for determination of cross-sectional area (CSA), specific force (Po/CSA) and unloaded shortening velocity (Vo) at 12 degrees C and maximum activation. Fibres were classified on the basis of their MHC isoform content determined by SDS-PAGE in three pure fibre types (1, 2A and 2X) and two hybrid fibre types (1-2A and 2AX). Whereas the CSA of individual muscle fibres did not change, Po/CSA was significantly higher in both type 1 and type 2A fibres post training. Vo of type 1 fibres was significantly higher post-training, whereas no change in Vo was observed in type 2A fibres. The number of pure type 2X fibres was very low especially post-training and did not enable a statistically significant comparison. The data suggest that in elderly women moderate and prolonged RT: (1) can determine similar adaptations in MHC distribution of skeletal muscle to those expected in young subjects; (2) can improve function of muscle fibres. [ABSTRACT FROM AUTHOR]

Unloaded inactivity induces atrophy and functional deconditioning of skeletal muscle, especially in the lower extremities. Information is scarce, however, regarding the effect of unloaded inactivity on muscle size and function about the hip. Regional bone loss has been demonstrated in hips and knees of elderly orthopaedic patients, as quantified by computerized tomography (CT). This method remains to be validated in healthy individuals rendered inactive, including real or simulated weightlessness. In this study, ten healthy males were subjected to 5 weeks of experimental bedrest and five matched individuals served as ambulatory controls. Maximum voluntary isometric hip and knee extension force were measured using the strain gauge technique. Cross-sectional area (CSA) of hip, thigh and calf muscles, and radiological density (RD) of the proximal tibial bone were measured using CT. Bedrest decreased ( P < 0.05) average (SD) muscle strength by 20 (8)% in knee extension, and by 22 (12)% in hip extension. Bedrest induced atrophy ( P < 0.05) of extensor muscles in the gluteal region, thigh and calf, ranging from 2 to 12%. Atrophy was more pronounced in the knee extensors [9 (4)%] and ankle plantar flexors [12 (3)%] than in the gluteal extensor muscles [2 (2)%]. Bone density of the proximal tibia decreased ( P < 0.05) by 3 (2)% during bedrest. Control subjects did not show any temporal changes in muscle or bone indices ( P > 0.05), when examined at similar time intervals. The present findings of a substantial loss in hip extensor strength and a smaller, yet significant atrophy of these muscles, demonstrate that hip muscle deconditioning accompanies losses in thigh and calf muscle mass after bedrest. This suggests that comprehensive quantitative studies on impaired locomotor function after inactivity should include all joints of the lower extremity. Our results also demonstrate that a decreased RD, indicating bone mineral loss, can be shown already after 5 weeks of unloaded bedrest, using a standard CT technique. [ABSTRACT FROM AUTHOR]

Repeated trials of hypercapnic exercise [deltaPET CO2 = 7 (1) mmHg] augment the increase in inspired minute ventilation and tidal volume (V(T)) in the early phase of subsequent trials of unencumbered exercise alone. The increase in V(T) in the first 20 s of exercise was correlated to the increase in V(T) evoked during hypercapnic exercise trials, suggesting that the evoked increase in V(T) during conditioning may be a factor in mediating associative conditioning. To test this hypothesis, inspiratory resistive loading (IRL) was employed to evoke an increase in V(T) [deltaV(T) = 0.4 (0.1) I(BTPS)] during conditioning exercise trials [IRL + EX; deltaP(ET)CO2 = 2 (l) mmHg]. IRL + EX associative conditioning elicited a significant augmentation of the early minute ventilation (+46%) and V(T) (+100%) responses to subsequent unencumbered exercise. The latter was correlated to the evoked increase in V(T) during associative conditioning with IRL + EX. The results support the hypothesis that an evoked increase in V(T) during associative conditioning could be a factor in eliciting long-term modulation of minute ventilation in subsequent unencumbered exercise. The results further indicated that the modulation of ventilation early in exercise is not due to sensitisation to repeated trials of either IRL or exercise alone. Associative conditioning may shape the ventilatory response to exercise through a process of motor learning. Data are presented as mean (SEM) unless otherwise stated. [ABSTRACT FROM AUTHOR]