This study investigated the effects of frequent low-load ischemic resistance exercise performed to failure on quadriceps size and performance, muscle activation, oxygen kinetics and cardiovascular responses. Ten healthy males performed knee-extension exercise for 4 weeks (4 sessions/week) at 15% maximal voluntary muscle contraction (MVC). One leg was trained with free blood flow (C-leg) while in the other leg (I-leg) ischemia was induced by an inflatable cuff (≥230 mmHg). Quadriceps cross-sectional area (CSA) of the I-leg increased by 3.4% (P<0.05). A tendency for smaller increase in muscle CSAs at the cuff level was observed. MVC force did not change in either leg, whereas the number of repetitions during exercise test to failure increased (P<0.01) by 63% in I-leg and 36% in C-leg. The decrease in muscle oxygenated hemoglobin concentration acquired by NIRS was attenuated (P<0.01) by 56% in I-leg and 21% in C-leg. Electromyographic amplitude of rectus femoris in I-leg was ∼45% lower (P<0.025) during the ischemic test. Also, ∼9% increase (P<0.05) in pre-exercise diastolic pressure was observed. In conclusion, substantial gains in muscle endurance capacity were induced, which were associated with enhanced muscle oxygen delivery. The potential negative effects of ischemic exercise with high cuff pressure on muscle and nerve and on arterial pressure regulation need further investigation.

Surgical ACL reconstruction performed with a tourniquet induces compression and ischemic stress of the quadriceps femoris (QF) muscle which can accelerate postoperative weakness. Given that low-load blood flow restricted (BFR) exercise is potent in enhancing muscle oxygenation and vascular function, we hypothesized that short-term preconditioning with low-load BFR exercise can attenuate QF muscle endurance deterioration in the postoperative period. Twenty subjects undergoing arthroscopic ACL reconstruction performed 5 exercise sessions in the last 8 days prior to surgery. They were assigned into either BFR group, performing low-load BFR knee-extension exercise, or SHAM-BFR group, replicating equal training volume with sham occlusion. Blood flow (near-infrared spectroscopy) and surface EMG of QF muscle during sustained isometric contraction at 30% of maximal voluntary isometric contraction (MVIC) torque performed to volitional failure were measured prior to the intervention and again 4 and 12 weeks after surgery. There was an overall decrease (p = 0.033) in MVIC torque over time, however, no significant time-group interaction was found. The time of sustained QF contraction shortened (p = 0.002) in SHAM-BFR group by 97 ± 85 s at week 4 and returned to preoperative values at week 12. No change in the time of sustained contraction was detected in BFR group at any time point after surgery. RMS EMG amplitude increased (p = 0.009) by 54 ± 58% at week 4 after surgery in BFR group only. BFm increased (p = 0.004) by 52 ± 47% in BFR group, and decreased (p = 0.023) by 32 ± 19% in SHAM-BFR group at week 4 after surgery. Multivariate regression models of postoperative changes in time of sustained QF contraction revealed its high correlation (R2 = 0.838; p < 0.001) with changes in BFm and RMS EMG in the SHAM-BFR group, whereas no such association was found in the BFR group. In conclusion, enhanced endurance of QF muscle was triggered by combination of augmented muscle fiber recruitment and enhanced muscle perfusion. The latter alludes to a preserving effect of preconditioning with BFR exercise on density and function of QF muscle microcirculation within the first 4 weeks after ACL reconstruction.

No abstract

Cutaneous temperature sensitivity was tested in 13 male subjects prior to, during and after they breathed either a hypocapnic hypoxic (HH), or a normocapnic hypoxic (NH) breathing mixture containing 10% oxygen in nitrogen. Normocapnia was maintained by adding carbon dioxide to the inspired gas mixture. Cutaneous thresholds for thermal sensation were determined by a thermosensitivity testing device positioned on the plantar side of the first two toes on one leg. Heart rate, haemoglobin saturation, skin temperature at four sites (arm, chest, thigh, calf) and adapting temperature of the skin (T(ad); degrees centigrade), i.e. the temperature of the toe skin preceding a thermosensitivity test, were measured at minute intervals. Tympanic temperature (T(ty); degrees centigrade) was measured prior to the initial normoxic thermosensitivity test, during the hypoxic exposure and after the completion of the final normoxic thermosensitivity test. End-tidal carbon dioxide fraction and minute inspiratory volume were measured continuously during the hypoxic exposure. Ambient temperature, T(ty), T(ad) and mean skin temperature remained similar in both experimental conditions. Cutaneous sensitivity to cold decreased during both HH (P<0.001) and NH conditions (P<0.001) as compared with the tests undertaken pre- and post-hypoxia. No similar effect was observed for cutaneous sensitivity to warmth. The results of the present study suggest that sensitivity to cold decreases during the hypoxic exposure due to the effects associated with hypoxia rather than hypocapnia. Such alteration in thermal perception may affect the individual's perception of thermal comfort and consequently attenuate thermoregulatory behaviour during cold exposure at altitude.

The effect of acute and 23 days of intermittent exposures to normobaric hypoxia on the forehead sweating response during steady-state exercise was investigated. Eight endurance athletes slept in a normobaric hypoxic room for a minimum of 8 h per day at a simulated altitude equivalent to 2,700 m for 23 days (sleep high-train low regimen). Peak oxygen uptake (VO2(peak)) and peak work rate (WR(peak)) were determined under normoxic (20.9%O(2)) and hypoxic (13.5%O(2)) conditions prior to (pre-IHE), and immediately after (post-IHE) the intermittent hypoxic exposures (IHE). Also, each subject performed three 30-min cycle-ergometry bouts: (1) normoxic exercise at 50% WR(peak) attained in normoxia (control trial; CT); (2) hypoxic exercise at 50% WR(peak) attained in hypoxia (hypoxic relative trial; HRT) and (3) hypoxic exercise at the same absolute work rate as in CT (hypoxic absolute trial; HAT). Exposure to hypoxia induced a 33 and 37% decrease (P < 0.001) in (VO2(peak)) pre-IHE and post-IHE, respectively. Despite similar relative oxygen uptake during HAT pre-IHE and post-IHE, the ratings of perceived whole-body exertion decreased substantially (P < 0.05) post-IHE. Pre-IHE the sweat secretion on the forehead (m(sw)f) was greater (P < 0.01) in the HAT (2.60 (0.80) mg cm(-2) min(-1)) compared to the other two trials (CT = 1.87 (1.09) mg cm(-2) min(-1); HRT = 1.57 (0.82) mg cm(-2) min(-1)) despite a similar exercise-induced elevation in body temperatures, resulting in an augmented (P < 0.01) gain of the sweating response (m(sw)f/Delta T(re)). The augmented (m(sw)f) and m(sw)f/Delta T(re) during the HAT were no longer evident post-IHE. Thus, it appears that exercise sweating on the forehead is potentiated by acute exposure to hypoxia, an effect which can be abolished by 23 days of intermittent hypoxic exposures.