PurposeWe evaluated the effect of different water immersion (WI) temperatures on post-exercise cardiac parasympathetic reactivation.MethodsEight young, physically active men participated in four experimental conditions composed of resting (REST), exercise session (resistance and endurance exercises), post-exercise recovery strategies, including 15 min of WI at 15°C (CWI), 28°C (TWI), 38°C (HWI) or control (CTRL, seated at room temperature), followed by passive resting. The following indices were assessed before and during WI, 30 min post-WI and 4 hours post-exercise: mean R-R (mR-R), the natural logarithm (ln) of the square root of the mean of the sum of the squares of differences between adjacent normal R–R (ln rMSSD) and the ln of instantaneous beat-to-beat variability (ln SD1).ResultsThe results showed that during WI mRR was reduced for CTRL, TWI and HWI versus REST, and ln rMSSD and ln SD1 were reduced for TWI and HWI versus REST. During post-WI, mRR, ln rMSSD and ln SD1 were reduced for HWI versus REST, and mRR values for CWI were higher versus CTRL. Four hours post exercise, mRR was reduced for HWI versus REST, although no difference was observed among conditions.ConclusionsWe conclude that CWI accelerates, while HWI blunts post-exercise parasympathetic reactivation, but these recovery strategies are short-lasting and not evident 4 hours after the exercise session.

Obesity is now considered to be an inflammatory condition associated with many pathological consequences, including insulin resistance. It is proposed that insulin resistance contributes to the aggravation of the inflammatory dysfunction in obesity. The effect of obesity on the percentage of monocytes was previously observed in class II and III obese individuals who presented other alterations in addition to insulin resistance. In this study we observed that insulin-resistant obese individuals, but not insulin-sensitive ones, had an increased percentage of CD14(+) CD16(+) monocytes. This fact shows that a dysfunction of the monocyte percentage in class I obese individuals is only seen when this condition is associated with insulin resistance.

This study investigated whether an acute session of high-intensity interval training (HIIT) is sufficient to alter lymphocyte function and redox status. Sixteen young healthy men underwent a HIIT session on a cycloergometer, consisting of eight bouts of 1 min at 90–100% of peak power, with 75 seconds of active recovery at 30 W between bouts. Venous blood was collected before, immediately after, and 30 minutes after the HIIT session. In response to Staphylococcus aureus superantigen B (SEB) stimulation, lymphocyte proliferation decreased and the IL-2 concentration increased after the HIIT session. However, the HIIT session had no effect on lymphocyte proliferation or IL-2 response to phytohemagglutinin stimulation. The HIIT session also induced lymphocyte redox imbalance, characterized by an increase in the concentration of thiobarbituric acid reactive substances and a decrease in the activity of the antioxidant enzyme catalase. Lymphocyte viability was not affected by the HIIT session. The frequencies of CD25+ and CD69+ T helper and B lymphocytes in response to superantigen stimulation were lower after exercise, suggesting that superantigen-induced lymphocyte activation was reduced by HIIT. However, HIIT also led to a reduction in the frequency of CD4+ and CD19+ cells, so the frequencies of CD25+ and CD69+ cells within the CD4 and CD19 cell populations were not affected by HIIT. These data indicate that the reduced lymphocyte proliferation observed after HIIT is not due to reduced early lymphocyte activation by superantigen. Our findings show that an acute HIIT session promotes lymphocyte redox imbalance and reduces lymphocyte proliferation in response to superantigenic, but not to mitogenic stimulation. This observation cannot be explained by alteration of the early lymphocyte activation response to superantigen. The manner in which lymphocyte function modulation by an acute HIIT session can affect individual immunity and susceptibility to infection is important and requires further investigation.

This study sought to evaluate the effects of a single session of exercise on the expression of Hsp70, of c-jun N-terminal kinase (JNK), and insulin receptor substrate 1 serine 612 (IRS(ser612)) phosphorylation in the skeletal muscle of obese and obese insulin-resistant patients. Twenty-seven volunteers were divided into three experimental groups (eutrophic insulin-sensitive, obese insulin-sensitive, and obese insulin-resistant) according to their body mass index and the presence of insulin resistance. The volunteers performed 60 min of aerobic exercise on a cycle ergometer at 60 % of peak oxygen consumption. M. vastus lateralis samples were obtained before and after exercise. The protein expressions were evaluated by Western blot. Our findings show that compared with paired eutrophic controls, obese subjects have higher basal levels of p-JNK (100 ± 23 % vs. 227 ± 67 %, p = 0.03) and p-IRS-1(ser612) (100 ± 23 % vs. 340 ± 67 %, p < 0.001) and reduced HSP70 (100 ± 16 % vs. 63 ± 12 %, p < 0.001). The presence of insulin resistance results in a further increase in p-JNK (460 ± 107 %, p < 0.001) and a decrease in Hsp70 (46 ± 5 %, p = 0.006), but p-IRS-1(ser612) levels did not differ from obese subjects (312 ± 73 %, p > 0.05). Exercise reduced p-JNK in obese insulin-resistant subjects (328 ± 33 %, p = 0.001), but not in controls or obese subjects. Furthermore, exercise reduced p-IRS-1(ser612) for both obese (122 ± 44 %) and obese insulin-resistant (185 ± 36 %) subjects. A main effect of exercise was observed in HSP70 (p = 0.007). We demonstrated that a single session of exercise promotes changes that characterize a reduction in cellular stress that may contribute to exercise-induced increase in insulin sensitivity.

Various post-exercise strategies have been proposed to accelerate recovery during periods of training. However, the effects of water immersion (WI) temperature on recovery amid multiple daily exercise bouts are not well investigated. PURPOSE: To evaluate the effects of cold and warm water immersion temperatures between acute exercise bouts vs. no WI recovery on running performance. METHODS: Nine recreationally trained men (age: 24.0 ± 6.0 years old) participated in four experimental sessions using a crossover design. Each experimental session consisted of unilateral eccentric knee flexion exercise and 90 min of treadmill running at 70% of peak oxygen consumption followed by 15 min of WI at 15°C, 28°C or 38°C or passive recovery seated at room temperature (CON). Four hours following WI or CON, subjects completed a 5 km running time trial. Rectal temperature (Trec), heart rate, and excess post-exercise oxygen consumption (EPOC) were measured. RESULTS: Statistical analyses indicated that time trial performance was not affected by post-exercise recovery by WI (P > .05). The magnitude-based inferences indicated that 15°C (+ 3.6 ± 7.8%) likely and 28°C (+ 3.2 ± 7.5%) possibly improved recovery compared with CON, while the effect of 38°C (-0.1 ± 12.3%) on recovery was unclear. During WI, heart rate and rectal temperature were not different from CON, but EPOC was higher in 15°C and 28°C compared to CON. Trec in 15°C was lower than CON from the 15th min post WI. EPOC was also greater in 15°C post WI compared to CON. CONCLUSION: WI at 15°C and 28°C following acute exercise likely and possibly, respectively, improved subsequent 5 km running time trial performance. We speculate that the faster recovery in core temperature post-exercise may underlie these improvements in recovery.

This study evaluated the effect of an acute high-intensity interval exercise (HIIE) session on the function of human neutrophils. Twelve sedentary men performed a HIIE session (8 bouts of 60 s at 90% of peak power, intercalated with 75 s of active recovery at 30 W). Neutrophils were collected before, 30 min and 24 h after the exercise session for the evaluation of phagocytic capacity, expression of phagocytic receptors, reactive oxygen species generation, and redox status. 24 h after the HIIE session, an increase was observed in both neutrophil phagocytic capacity and yeast-induced generation of reactive oxygen species, which indicates neutrophil priming in response to an acute HIIE session. Neutrophils also presented an increase in superoxide dismutase activity 24 h after the exercise. Improvement in neutrophil function was accompanied by increased serum levels of IL-8 and increased concentration of plasma lactate dehydrogenase. Our findings show a late activating effect of one HIIE session on neutrophils. We propose that priming of neutrophils by HIIE may play a role in skeletal muscle inflammation after exercise.

High-intensity interval training (HIIT) induces vascular adaptations that might be attenuated by postexercise cold-water immersion (CWI). Circulating angiogenic cells (CAC) participate in the vascular adaptations and circulating endothelial cells (CEC) indicate endothelial damage. CAC and CEC are involved in vascular adaptation. Therefore, the aim of the study was to investigate postexercise CWI during HIIT on CAC and CEC and on muscle angiogenesis-related molecules. Seventeen male subjects performed 13 HIIT sessions followed by 15 min of passive recovery (n = 9) or CWI at 10 °C (n = 8). HIIT comprised cycling (8–12 bouts, 90%–110% peak power). The first and the thirteenth sessions were similar (8 bouts at 90% of peak power). Venous blood was drawn before exercise (baseline) and after the recovery strategy (postrecovery) in the first (pretraining) and in the thirteenth (post-training) sessions. For CAC and CEC identification lymphocyte surface markers (CD133, CD34, and VEGFR2) were used. Vastus lateralis muscle biopsies were performed pre- and post-training for protein (p-eNOSser1177) and gene (VEGF and HIF-1) expression analysis related to angiogenesis. CAC was not affected by HIIT or postexercise CWI. Postexercise CWI increased acute and baseline CEC number. Angiogenic protein and genes were not differently modulated by post-CWI. HIIT followed by either recovery strategy did not alter CAC number. Postexercise CWI increased a marker of endothelial damage both acutely and chronically, suggesting that this postexercise recovery strategy might cause endothelial damage. Novelty HIIT followed by CWI did not alter CAC. HIIT followed by CWI increased CEC. Postexercise CWI might cause endothelial damage.

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