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Purpose: Protein supplementation has been proposed as an effective dietary strategy for maintaining or increasing skeletal muscle mass and improving physical performance in middle-aged and older adults. Diabetes mellitus exacerbates muscle mass loss, leading to many older adults with type 2 diabetes mellitus (T2DM) experiencing sarcopenia, and vice versa. Our objective was to assess the impact of increased dietary protein intake on muscle mass, strength, physical performance, and the progression of T2DM in middle-aged and older adults diagnosed with this condition. Methods: A 12-week randomized, controlled, parallel pilot study was conducted with 26 patients diagnosed with T2DM and had either low muscle mass, or low muscle strength or poor physical performance (age > 55 years old), aiming to investigate the effects of a protein-rich diet in sarcopenic and metabolic markers. The control group received 0.8–1.0 g/kg/day, while the intervention group received 1.2–1.5 g/kg/day of protein respectively. Body composition, muscle mass/strength and biochemical parameters were measured before and after the intervention period. Results: Different kinetics of skeletal muscle index (SMI), appendicular lean mass (ALM), hand grip strength (HGS), gait speed (GS) and standing balance (SB) (p < 0.05) were observed between two groups. Specifically, the intervention group showed a significant improvement in HGS (p < 0.001) and physical performance (timed-up-and-go, p < 0.001; GS, p = 0.011; SB, p = 0.022), while the control group had its ALM (p = 0.014), SMI (p = 0.011) and HGS (p = 0.011) significantly reduced. The kinetics of metabolic markers indices was similar for both groups. Conclusion: Current recommendation for protein intake (0.8–1 g/kg/day) is certainly not enough to ameliorate the muscle mass loss in middle age and older adults’ individuals with T2DM. In contrast, protein intake of 1.2–1.5 g/kg/day seems to be a more appropriate recommendation to combat upcoming sarcopenia, nonetheless the progression of T2DM was not interrupted. [ABSTRACT FROM AUTHOR]

Despite its comparatively limited size in humans, spleen has been shown able to expel red-blood cells in the circulation and thus augment blood oxygen-carrying capacity under certain physiologic conditions. In the present state-of-the-art review, the short- and long-term regulation of spleen volume will be discussed. With regards to the physiological mechanism underlying spleen contraction, sympathetic activation stands as the prime contributor to the response. A dose-dependent relationship between specific interventions of apnea, exercise and hypoxia (imposed separately or in combination) and spleen contraction alleges to the trainability of the spleen organ. The trainability of the spleen is further substantiated by virtue of cross-sectional and longitudinal studies reporting robust increases in both organ volume at rest and subsequent spleen contraction. Alternative ways to assess the relationship between hematologic gains and the magnitude of spleen contraction (i.e., the reduction of spleen volume) will be presented herein. In extension of changes in the conventional measures of hemoglobin concentration and hematocrit, assessment of hemoglobin mass and total blood volume using the (safe, low-cost and time-efficient) CO-rebreathing technique could deepen scientific knowledge on the efficiency of human spleen contraction. [ABSTRACT FROM AUTHOR]

Purpose: This study examined the physiological responses of ten elite divers to normal breathing (BHn), glossopharyngeal inhalation (BHi), and complete exhalation (BHe) prior to five maximal breath-hold (BH) efforts.Breath-hold time (BHT), hemological variables, mean arterial pressure (MAP), other hemodynamic indices, and diaphragmatic activity (DA) were recorded. During BHs, phases were identified as easy-going (EPh: minimal DA), struggling (SPh: increased DA), PhI (MAP transition), PhII (MAP stabilization), and PhIII (steep MAP increase).BHi significantly extended BHT (309.14 ± 12.91 s) compared to BHn (288.77 ± 10.99 s) and BHe (151.18 ± 10.94 s) (P = 0.001). BHT, EPh, and SPh in BHi increased by 7.05%, 2.57%, and 11.08% over BHn, respectively. PhIII appeared earlier in BHe than in other conditions (P < 0.001) and accounted for 47.07%, 44.96%, and 60.18% of BHT in BHn, BHi, and BHe, respectively. SPh comprised 47.10%, 46.01%, and 45.13% of BHT in BHn, BHi, and BHe, respectively, with SPh onset coinciding with PhIII onset in BHn and BHi but not in BHe. Bradycardia was more pronounced in BHe, maintaining better stroke volume. No significant differences in red blood cells or maximal MAP were noted across conditions.Glossopharyngeal inhalation improves BHT and extends EPh and SPh durations. PhIII onset is linked to SPh in BHn and BHi but not in BHe. BHe triggers an earlier MAP rise, leading to stronger parasympathetic responses. Despite similar maximal MAP across conditions, the higher BHT and tissue hypoxemia in BHi and BHn suggest MAP is a key limiting factor in apnoea.Methods: This study examined the physiological responses of ten elite divers to normal breathing (BHn), glossopharyngeal inhalation (BHi), and complete exhalation (BHe) prior to five maximal breath-hold (BH) efforts.Breath-hold time (BHT), hemological variables, mean arterial pressure (MAP), other hemodynamic indices, and diaphragmatic activity (DA) were recorded. During BHs, phases were identified as easy-going (EPh: minimal DA), struggling (SPh: increased DA), PhI (MAP transition), PhII (MAP stabilization), and PhIII (steep MAP increase).BHi significantly extended BHT (309.14 ± 12.91 s) compared to BHn (288.77 ± 10.99 s) and BHe (151.18 ± 10.94 s) (P = 0.001). BHT, EPh, and SPh in BHi increased by 7.05%, 2.57%, and 11.08% over BHn, respectively. PhIII appeared earlier in BHe than in other conditions (P < 0.001) and accounted for 47.07%, 44.96%, and 60.18% of BHT in BHn, BHi, and BHe, respectively. SPh comprised 47.10%, 46.01%, and 45.13% of BHT in BHn, BHi, and BHe, respectively, with SPh onset coinciding with PhIII onset in BHn and BHi but not in BHe. Bradycardia was more pronounced in BHe, maintaining better stroke volume. No significant differences in red blood cells or maximal MAP were noted across conditions.Glossopharyngeal inhalation improves BHT and extends EPh and SPh durations. PhIII onset is linked to SPh in BHn and BHi but not in BHe. BHe triggers an earlier MAP rise, leading to stronger parasympathetic responses. Despite similar maximal MAP across conditions, the higher BHT and tissue hypoxemia in BHi and BHn suggest MAP is a key limiting factor in apnoea.Results: This study examined the physiological responses of ten elite divers to normal breathing (BHn), glossopharyngeal inhalation (BHi), and complete exhalation (BHe) prior to five maximal breath-hold (BH) efforts.Breath-hold time (BHT), hemological variables, mean arterial pressure (MAP), other hemodynamic indices, and diaphragmatic activity (DA) were recorded. During BHs, phases were identified as easy-going (EPh: minimal DA), struggling (SPh: increased DA), PhI (MAP transition), PhII (MAP stabilization), and PhIII (steep MAP increase).BHi significantly extended BHT (309.14 ± 12.91 s) compared to BHn (288.77 ± 10.99 s) and BHe (151.18 ± 10.94 s) (P = 0.001). BHT, EPh, and SPh in BHi increased by 7.05%, 2.57%, and 11.08% over BHn, respectively. PhIII appeared earlier in BHe than in other conditions (P < 0.001) and accounted for 47.07%, 44.96%, and 60.18% of BHT in BHn, BHi, and BHe, respectively. SPh comprised 47.10%, 46.01%, and 45.13% of BHT in BHn, BHi, and BHe, respectively, with SPh onset coinciding with PhIII onset in BHn and BHi but not in BHe. Bradycardia was more pronounced in BHe, maintaining better stroke volume. No significant differences in red blood cells or maximal MAP were noted across conditions.Glossopharyngeal inhalation improves BHT and extends EPh and SPh durations. PhIII onset is linked to SPh in BHn and BHi but not in BHe. BHe triggers an earlier MAP rise, leading to stronger parasympathetic responses. Despite similar maximal MAP across conditions, the higher BHT and tissue hypoxemia in BHi and BHn suggest MAP is a key limiting factor in apnoea.Conclusion: This study examined the physiological responses of ten elite divers to normal breathing (BHn), glossopharyngeal inhalation (BHi), and complete exhalation (BHe) prior to five maximal breath-hold (BH) efforts.Breath-hold time (BHT), hemological variables, mean arterial pressure (MAP), other hemodynamic indices, and diaphragmatic activity (DA) were recorded. During BHs, phases were identified as easy-going (EPh: minimal DA), struggling (SPh: increased DA), PhI (MAP transition), PhII (MAP stabilization), and PhIII (steep MAP increase).BHi significantly extended BHT (309.14 ± 12.91 s) compared to BHn (288.77 ± 10.99 s) and BHe (151.18 ± 10.94 s) (P = 0.001). BHT, EPh, and SPh in BHi increased by 7.05%, 2.57%, and 11.08% over BHn, respectively. PhIII appeared earlier in BHe than in other conditions (P < 0.001) and accounted for 47.07%, 44.96%, and 60.18% of BHT in BHn, BHi, and BHe, respectively. SPh comprised 47.10%, 46.01%, and 45.13% of BHT in BHn, BHi, and BHe, respectively, with SPh onset coinciding with PhIII onset in BHn and BHi but not in BHe. Bradycardia was more pronounced in BHe, maintaining better stroke volume. No significant differences in red blood cells or maximal MAP were noted across conditions.Glossopharyngeal inhalation improves BHT and extends EPh and SPh durations. PhIII onset is linked to SPh in BHn and BHi but not in BHe. BHe triggers an earlier MAP rise, leading to stronger parasympathetic responses. Despite similar maximal MAP across conditions, the higher BHT and tissue hypoxemia in BHi and BHn suggest MAP is a key limiting factor in apnoea.Graphical abstract: This study examined the physiological responses of ten elite divers to normal breathing (BHn), glossopharyngeal inhalation (BHi), and complete exhalation (BHe) prior to five maximal breath-hold (BH) efforts.Breath-hold time (BHT), hemological variables, mean arterial pressure (MAP), other hemodynamic indices, and diaphragmatic activity (DA) were recorded. During BHs, phases were identified as easy-going (EPh: minimal DA), struggling (SPh: increased DA), PhI (MAP transition), PhII (MAP stabilization), and PhIII (steep MAP increase).BHi significantly extended BHT (309.14 ± 12.91 s) compared to BHn (288.77 ± 10.99 s) and BHe (151.18 ± 10.94 s) (P = 0.001). BHT, EPh, and SPh in BHi increased by 7.05%, 2.57%, and 11.08% over BHn, respectively. PhIII appeared earlier in BHe than in other conditions (P < 0.001) and accounted for 47.07%, 44.96%, and 60.18% of BHT in BHn, BHi, and BHe, respectively. SPh comprised 47.10%, 46.01%, and 45.13% of BHT in BHn, BHi, and BHe, respectively, with SPh onset coinciding with PhIII onset in BHn and BHi but not in BHe. Bradycardia was more pronounced in BHe, maintaining better stroke volume. No significant differences in red blood cells or maximal MAP were noted across conditions.Glossopharyngeal inhalation improves BHT and extends EPh and SPh durations. PhIII onset is linked to SPh in BHn and BHi but not in BHe. BHe triggers an earlier MAP rise, leading to stronger parasympathetic responses. Despite similar maximal MAP across conditions, the higher BHT and tissue hypoxemia in BHi and BHn suggest MAP is a key limiting factor in apnoea. [ABSTRACT FROM AUTHOR]

We tested the hypothesis that menthol application would reduce the magnitude and initiation of sweating via excitation of cold-sensitive afferent pathways and concurrently via a cross-inhibition of heat loss pathways in acclimatized (swimmers, SW) and non acclimatized (control, CON) subjects in cool water. It was expected this effect to be exaggerated in SW subjects. Eight SW and eight CON subjects cycled at 60% of their VO(2)max, as long as to reach 38 degrees C in rectal temperature (Tre), without or with (4.6 g per 100 ml of water) all-body application of menthol sediment. Heart rate (HR), Tre, sweating rate (SwR), the proximal-distal skin temperature gradient (TSk(f-f)), and oxygen consumption (VO(2)) were measured continuously. VO(2) and HR were similar between groups and conditions. Menthol increased TSk(f-f), Tre threshold for SwR [+0.32 (0.01) degrees C] and Tre gain, while menthol reduced exercise time by 8.1 (4.1) min. SW group showed higher changes in Tre threshold for SwR [+0.50 (0.01) degrees C for SW vs. +0.13 (0.03) degrees C for CON], higher Tre gain, lower time for Tre increase and shorter exercise time [-10.7 (7) min for SW vs. -4.9 (4) min for CON] in menthol condition. Upon exercise initiation, previously applied menthol on the skin seems to induce vasoconstriction, results in a delayed sweating, which in turn affects the rectal temperature. Acclimatized subjects showed higher delay in SwR and earlier rise in Tre, which most probably is due to the inter-group differences in cold receptors activity. [ABSTRACT FROM AUTHOR]

This study examined the role of muscle pump in the development of cardiovascular drift (CVdrift) during cycling. Twelve healthy males (23.4 +/- 0.5 years, mean +/- SE) exercised for 90 min with 40 and 80 pedal revolutions per minute (rpm) at the same oxygen consumption, in two separate days. CVdrift was developed in both conditions as indicated by the drop in stroke volume (SV) and the rise in heart rate (HR) from the 20th min onwards (Delta SV = -16.2 +/- 2.0 and -17.1 +/- 1.0 ml beat(-1); Delta HR = 18.3 +/- 2.0 and 17.5 +/- 3.0 beats min(-1) for 40 and 80 rpm, respectively, P < 0.05) but without difference between conditions. Mean cardiac output (CO2 rebreathing) was 14.7 +/- 0.3 l min(-1) and 15.0 +/- 0.3 l min(-1), and mean arterial pressure was 100.0 +/- 1.0 mmHg and 96.7 +/- 0.8 mmHg for 40 and 80 rpm, respectively, without significant changes over time, and without difference between conditions. Electromyographic activity (iEMG) was lower throughout exercise with 80 rpm (35.6 +/- 1.2% and 11.0 +/- 1.0% for 40 and 80 rpm, respectively). Similarly, total hemoglobin, determined with near-infrared spectroscopy (NIRS) was 58.0 +/- 0.8 (AU) for 40 rpm and 53.0 +/- 1.4 (arbitrary units) for 80 rpm, from 30th min onwards (P < 0.05), an indication of lower leg blood volume during the faster pedal rate condition. Thermal status (rectal and mean skin temperature), blood and plasma volume changes, blood lactate concentration, muscle oxygenation (NIRS signal) and the rate of perceived exertion were similar in the two trials. It seems that muscle pump is not an important factor for the development of CVdrift during cycling, at least under the present experimental conditions. [ABSTRACT FROM AUTHOR]

The aim of this study was to compare the cardiovascular responses to prolonged submaximal cycling and running. Eleven males [maximal oxygen uptake (VO2max): 3.58±0.15 l min–1 for running and 3.84±0.16 l min–1 for cycling; mean±SE] either cycled (C) or ran (R) for 90 min at 60% of mode-specific VO2max, on two randomly assigned occasions. Cardiac output declined after 85 min of exercise in C (–1.9±0.5 l min–1, P<0.01) but not in R, as a result of a more pronounced decrease in stroke volume in the former exercise mode (–22.7±3.8 ml beat–1 vs –14.3±1.9 ml beat–1, P<0.01) since heart rate did not differ between trials. Stroke volume responses were despite a higher level of dehydration (–3.3±0.2% in R vs –2.8±0.2% in C, P<0.05) and hyperthermia in R (39.6±0.1 vs 38.8±0.1°C in C at 90 min, P<0.01). Finally, mean skin blood flow was lower in R than C (72±8 vs 89±10%; P<0.05). In conclusion, stroke volume and cardiac output decline was more pronounced in cycling than in running despite lower dehydration and rectal temperature in the former exercise mode. [ABSTRACT FROM AUTHOR]

The aim of this investigation was to examine the effect of water ingestion on physiological responses to prolonged cycling (CYC) and running (RUN). A group of 11 men with mean (SEM) maximal oxygen uptake (&Vdot;O2max) 48.5 (1.8) ml·kg-1·min-1 on a cycle-ergometer and 52.1 (2.2) ml·kg-1·min-1 on a treadmill (P < 0.01) exercised for 90 min on four occasions, twice on each ergometer, at 60% of mode specific VO2max. No fluid was taken (D) in one trial on each ergometer, whereas 60% of fluid losses were replaced by drinking water in the other trial (W). In CYC, water ingestion attenuated the change in cardiac output (Δ&Qdot;c) and the reduction in stroke volume (ΔSV) [ΔSV: -22.7 (3.8) in D, -10.7 (2.9) ml·beat-1 in W, P < 0.01; Δ&Qdot;c: -1.9 (0.5) in D, -0.2 (0.4) l·min-1 in W at 85 min, P < 0.01], but did not affect rectal temperature [Tre at 90 min: 38.8 (0.1)°C in D, 38.7 (0.1)°C in W]. In contrast, fluid replacement reduced hyperthermia in RUN [Tre at 90 min: 39.6 (0.2) in D, 39.1 (0.2)°C in W, P < 0.01], and this was linked with a higher skin blood flow [RUN-W 88.9 (8.5), RUN-D 70.7 (8.4)%, P < 0.05]. The Δ&Qdot;c and ΔSV were also attenuated with water ingestion in this mode of exercise (P < 0.05). It is concluded that water ingestion improves physiological function in both cycling and running, but that the underlying mechanism is different in the two modes of exercise. [ABSTRACT FROM AUTHOR]