Abstract Purpose In this study, we investigated whether experimental knee pain alters lower limb kinematics and knee arthrokinematics during gait, and if this motor adaptation depends on the spatial characteristics of the painful stimulus. Methods Twenty-one participants walked on a treadmill for 60-s trials, either without stimulation or while experiencing painful electrical stimulation in the medial, lateral or anterior region of the knee. Perceived pain location was analyzed using pain drawing. Gait spatiotemporal parameters, lower limb kinematics, and dispersion of the knee helical axes on the sagittal plane were quantified for each trial and compared between conditions using ANOVAs with repeated measures or Friedman tests. Results Pain perception was localized in the area the stimulation was applied to. Compared to walking without pain, participants demonstrated reduced knee extension (1.5 ± 1.5 degrees, p = 0.002) and reduced hip extension (0.8 ± 1.1 degrees, p = 0.037) when pain was induced in the anterior region, but not medially or laterally. Anterior knee pain increased the mean distance of the helical axes during late stance (0.7 [0.3, 1.4], p = 0.010), while medial pain increased both mean distance (0.3 [0.1, 0.5], p = 0.037) and mean angle (1.2 ± 1.4, p = 0.010) during early swing. Conclusion Acute, experimental knee pain alters gait kinematics and increases the dispersion of the helical axis. These adaptations depend on the spatial characteristics of the painful stimulus. These adaptations may reflect an attempt of the central nervous system to protect the painful tissue while searching for a less painful movement strategy.

Abstract Purpose Acute exercise can transiently enhance cognitive flexibility. The cognitive demand of firefighters makes it relevant to understand if on-shift exercise could produce similar improvements in cognitive performance during subsequent occupational tasks. Metrics of heart rate variability (HRV), such as time- and frequency-domain outcomes, may shed light upon the influence exercise has on cognition, as they discern information related to cardiac autonomic (sympathetic/parasympathetic) function. We aimed to determine if acute resistance and aerobic exercise impact cognitive flexibility during occupational tasks and its relation to HRV. Methods 32 participants completed a baseline Wisconsin Card Sorting Task (WCST) and three experimental trials: resistance exercise (RE), aerobic exercise (AE), or a rested control (CON). An occupational task assessment (OTA) including four rounds of 10 deadlifts and a 0.15-mile sandbag carry in an environmental chamber (35 °C/50% humidity) was completed after each trial. The second round was followed by the WCST. Repeated measures ANOVAs were used to analyze differences by condition. Results For the WCST, total, perseverative, and non-perseverative errors did not differ (ps > 0.39). Time-domain HRV metrics were not different (ps > 0.05). All frequency-domain metrics, other than low-frequency power, were not different (ps > 0.24). Low-frequency power was lower based on condition (p = 0.03). Post hoc analysis showed low-frequency power was lower following AE compared to RE and CON. Conclusion Results suggest an acute bout of on-shift aerobic or resistance exercise may not impact cognitive flexibility during subsequent simulated occupational tasks, despite depressed metrics of heart rate variability following aerobic exercise.

Within human skeletal muscle, statin treatment leads to elevated levels of the glucocorticoid-induced leucine zipper (GILZ). Further, GILZ mediates the muscle-related side effects of statins. Physical exercise leads to GILZ suppression, in a mechanosensitive manner. Given that statin treatment is rarely tolerated by habitually exercising individuals due to statin-associated muscle symptoms (SAMS), it appears that the opposing regulation of GILZ facilitates this detrimental interaction of two key measures of cardiovascular prevention, specifically for exercise modalities with high muscle strain. Similarly, opposing regulation of atrophy associated genes (atrogenes) may be a further mechanism. If confirmed, these results might have implications for the exercise prescription of statin-users. A systematic search of the Gene Expression Omnibus (GEO) repository for studies reporting the acute effects of either endurance (END), conventional resistance (RT), or eccentric resistance training (ECC) was conducted. GILZ, as well as the expression of pivotal atrogenes (e.g., muscle atrophy F-box, cathepsin L, etc.) were quantified. 15 studies with 204 participants (22 females; 182 males) were included. RT resulted in the highest GILZ suppression, significantly differing from the expressional change after END ( - 0.46 ± 1.11 vs. - 0.07 ± 1.08), but not from ECC ( - 0.46 ± 1.11 vs. - 0.46 ± 0.95). Similar results were seen for various atrogenes. Our results strengthen the assumption that mechanical loading can be considered a key mediator of exercise-induced changes in GILZ and atrogene expression.

In an asymptomatic population, we investigated the relationships between glycated haemoglobin (HbA1c) and cartilage T2 relaxation time at the knee joint level. Fourteen and 17 participants with high and normal levels of HbA1c were recruited, respectively. A blood sample was used to determine the HbA1c level. T2 relaxation time (T2) of the superficial and deep parts of the femoral cartilage in the anterior, central, and posterior topographical sites was calculated using magnetic resonance (1.5T) images. Each participant completed a knee injury and osteoarthritis outcome score questionnaire (KOOS) and a series of biomechanical analyses while running at their self-selected speed. The group with a high level of HbA1c had a lower score of KOOS symptoms than the other group (P < 0.05). HbA1c was found to be negatively related to the KOOS symptoms score. The group with a high level of HbA1c had low T2 values in all of the investigated topographical sites of the knee femoral cartilage (P < 0.05 in all cases). T2 was negatively correlated with HbA1c levels in all investigated knee femoral cartilage regions. Our data suggest that the subjects with high levels of HbA1c were those with low knee joint symptoms and lower values of T2. These results indicate that HbA1c could be correlated with cartilage deterioration due to its ability to dehydrate collagen fibre, possibly acting as a risk factor for the development of osteoarthritis.

The present study examined the effects of gastric emptying rate and intestinal cell damage following a single session of endurance exercise under "hypoxic" or "normoxic" conditions at the same relative intensity. Eleven healthy males performed two trials on different days, consisting of a 60min run on a treadmill at 70% maximal running velocity (vMax) while inspiring hypoxic (FiO2: 14.5%; HYP) or normoxic air (FiO2: 20.9%; NOR). The average running velocity was 11.4 ± 0.7km/h in NOR and 10.8 ± 0.5km/h in HYP, respectively. Venous blood samples were collected to evaluate plasma intestinal fatty acid binding protein (I-FABP) as an indicator of exercise-induced intestinal cell damage. The gastric emptying rate was determined by the 13C-sodium acetate breath test. Running velocities at 70% vMax and arterial oxygen saturation were significantly lower under HYP than NOR (p < 0.001). Peak heart rate and rating of perceived exertion during exercise did not differ significantly between the trials. Maximum 13C excretion time (an indication of the gastric emptying rate) was significantly delayed in the HYP (NOR: 38.5 ± 5.0min, HYP: 45.5 ± 9.6min; p = 0.010). Furthermore, the score of nausea increased slightly, but increased significantly after exercise only in the HYP (p = 0.04). However, exercise-induced changes in plasma I-FABP, adrenaline, and noradrenaline concentrations did not differ significantly between the two trials. These results suggest that endurance exercise under hypoxic conditions impairs digestive function in the stomach compared to exercise under normoxic conditions performed at the same relative intensity.

Exercise training requires the careful application of training dose to maximize adaptation while minimizing the risk of illness and injury. High-intensity interval training (HIIT) is a potent method for improving health and fitness but generates substantial autonomic imbalance. Assuming a supine posture between intervals is a novel strategy that could enhance physiological readiness and training adaptations. This study aimed to establish the safety and feasibility of supine recovery within a HIIT session and explore its acute effects. Fifteen healthy, active males (18-34years) underwent assessment of cardiopulmonary fitness. Participants completed two identical HIIT treadmill sessions (4 x [3min at 95% VO2max, 3min recovery]) employing passive recovery in standing (STANDard) or supine (SUPER) posture between intervals. Heart rate variability (HRV), HRV recovery (HRVrec; lnRMSSD) and heart rate recovery at 1min (HRrec) were assessed using submaximal constant speed running tests (CST) completed prior to, immediately after and 24h following HIIT. No severe adverse events occurred with SUPER, and compliance was similar between conditions (100 ± 0%). The change in HRVrec from the CST pre-to-post-HIIT was not different between conditions (p = 0.38); however, HRrec was faster following SUPER (39 ± 7bpm) vs. STANDard (36 ± 5bpm). HRV 24h post-SUPER was also greater (3.56 ± 0.57ms) compared to STANDard (3.37 ± 0.42ms). Despite no differences in perceived exertion (p = 0.23) and blood lactate levels (p = 0.35) between SUPER and STANDard, average running HRs were lower (p = 0.04) with SUPER (174 ± 7bpm) vs. STANDard (176 ± 7bpm). Supine recovery within HIIT attenuates acute cardioautonomic perturbation and accelerates post-exercise vagal reactivation. SUPER enhances recovery of vagal modulation, potentially improving physiological preparedness 24h post-HIIT. Further research exploring the chronic effects of SUPER are now warranted.