Bouts Of Handgrip Exercise Research Articles

Skeletal Muscle Mitochondrial Plasticity Is Reduced In Liver Transplant Recipients

PURPOSE Sarcopenic obesity is a hallmark of liver transplant recipients, of which the mechanisms are not yet fully understood. Decline in mitochondrial plasticity could play a mechanistic role in muscle wasting, loss of strength, and increased adiposity via impaired energy substrate utilization. The purpose of this study is to determine if skeletal muscle mitochondrial plasticity is reduced in liver transplant (LT) recipients. METHODS In this prospective cohort study, 15 LT patients (Mean±SD; Age: 58±10 years; months since transplant: 55±81 months) and 10 age matched healthy controls (Age: 55±4 years), underwent assessment of mitochondrial oxidative capacity of the wrist flexor muscle group. Near infrared spectroscopy coupled with repeated, transient arterial occlusions, measured the recovery kinetics of oxygen consumption following a 10 second bout of hand grip exercise. Post exercise metabolic recovery rate constant was calculated and reported as an index of mitochondrial oxidative capacity. RESULTS Post exercise metabolic recovery rates were significantly greater in LT recipients (Mean±SEM; Recovery Time Constant: 72±7 s) compared to HC (51±4 s; p=0.03) indicative of diminished mitochondrial plasticity in this patient cohort (Figure 1). CONCLUSION Skeletal muscle mitochondrial plasticity is reduced in LT patients compared to matched healthy controls. Further investigations are warranted to determine the role of mitochondrial dysfunction in the development of sarcopenic obesity and frailty following LT.

Impaired brachial artery flow-mediated vasodilation in response to handgrip exercise-induced increases in shear stress in young smokers

Smoking is an established risk factor for cardiovascular disease. It has also been shown to result in endothelial dysfunction as assessed by flow-mediated dilation (FMD) in response to reactive hyperemia (RH)-induced increases in shear stress. Handgrip exercise (HGEX) is an emerging alternative method to increase shear stress for FMD assessment (HGEX-FMD) and the purpose of this study was to identify the impact of smoking on HGEX-FMD in young healthy subjects. Brachial artery RH-FMD and HGEX-FMD (10-minute bout of HGEX) was assessed in eight smokers (S) and 14 non-smokers (NS) (age 21 ± 2 years). Brachial artery diameter and mean blood velocity were assessed with echo and Doppler ultrasound, respectively. Shear stress was estimated by shear rate (SR = brachial artery blood velocity/diameter). The SR stimulus did not differ between groups for either test (RH-FMD (SR area under the curve until peak diameter measurement), p = 0.897; HGEX-FMD (average SR over 10-minute exercise bout), p = 0.599). The RH-FMD magnitude was not significantly different between groups (S: 7.7 ± 2.2% vs NS: 7.9 ± 2.4%, p = 0.838); however, the HGEX-FMD magnitude was significantly impaired in smokers (S: 6.1 ± 3.4% vs NS: 9.6 ± 3.6%, p = 0.037). In conclusion, HGEX-FMD assessment detected vascular dysfunction in young healthy smokers while RH-FMD did not. This suggests that HGEX-FMD may be useful in the early detection of smoking-induced impairments in endothelial function. Further research is required to explore this phenomenon in other populations and to isolate underlying mechanisms.

Exercise-mediated changes in conduit artery wall thickness in humans: role of shear stress

Episodic increases in shear stress have been proposed as a mechanism that induces training-induced adaptation in arterial wall remodeling in humans. To address this hypothesis in humans, we examined bilateral brachial artery wall thickness using high-resolution ultrasound in healthy men across an 8-wk period of bilateral handgrip training. Unilaterally, shear rate was attenuated by cuff inflation around the forearm to 60 mmHg. Grip strength, forearm volume, and girth improved similarly between the limbs. Acute bouts of handgrip exercise increased shear rate (P < 0.005) in the noncuffed limb, whereas cuff inflation successfully decreased exercise-induced increases in shear. Brachial blood pressure responses similarly increased during exercise in both the cuffed and noncuffed limbs. Handgrip training had no effect on baseline brachial artery diameter, blood flow, or shear rate but significantly decreased brachial artery wall thickness after 6 and 8 wk (ANOVA, P < 0.001) and wall-to-lumen ratio after week 8 (ANOVA, P = 0.005). The magnitude of decrease in brachial artery wall thickness and wall-to-lumen ratio after exercise training was similar in the noncuffed and cuffed arms. These results suggest that exercise-induced changes in shear rate are not obligatory for arterial wall remodeling during a period of 8 wk of exercise training in healthy humans.

Shear Stress Mediates Endothelial Adaptations to Exercise Training in Humans

Although episodic changes in shear stress have been proposed as the mechanism responsible for the effects of exercise training on the vasculature, this hypothesis has not been directly addressed in humans. We examined brachial artery flow-mediated dilation, an index of NO-mediated endothelial function, in healthy men in response to an acute bout of handgrip exercise and across an 8-week period of bilateral handgrip training. Shear stress responses were attenuated in one arm by cuff inflation to 60 mm Hg. Similar increases were observed in grip strength and forearm volume and girth in both limbs. Acute bouts of handgrip exercise increased shear rate (P<0.005) and flow-mediated dilation percentage (P<0.05) in the uncuffed limb, whereas no changes were evident in the cuffed arm. Handgrip training increased flow-mediated dilation percentage in the noncuffed limb at weeks 2, 4, and 6 (P<0.001), whereas no changes were observed in the cuffed arm. Brachial artery peak reactive hyperemia, an index of resistance artery remodeling, progressively increased with training in the noncuffed limb (P<0.001 and 0.004); no changes were evident in the cuffed arm. Neither acute nor chronic shear manipulation during exercise influenced endothelium-independent glyceryl trinitrate responses. These results demonstrate that exercise-induced changes in shear provide the principal physiological stimulus to adaptation in flow-mediated endothelial function and vascular remodeling in response to exercise training in healthy humans.

The Impact Of Exercise On Derived Central Measures Obtained From The Sphygmocor Device

PURPOSE: To investigate whether measures derived from the SphygmoCor device and its associated transfer function are influenced by exercise-induced alterations in vascular tone. To do this, measurements were taken from either the exercised or the contra-lateral non-exercised limb, during repeated and identical incremental hand-grip protocols. METHODS: Eight male subjects performed 3, 3-minute bouts of handgrip exercise, on two occasions. The exercise intensities were set at: 3kg and 5kg, with a final 1.5kg bout performed during cuff ischaemia (1.5Isch). Blood pressure waveforms were recorded from the radial artery of either the exercised or non-exercised limb using applanation tonometry (SphygmoCor) during a 90 s rest period immediately after each exercise bout. Central blood pressures and augmentation indices, an index of arterial stiffness, were derived using the peripheral waveform and the inbuilt SphygmoCor transfer function (TF). RESULTS: Augmentation index (AIx) was consistently ∼10% higher in the exercised arm during all trials compared to the non-exercised lim. Similarly, there was a consistent and significant difference (∼3 mmHg; P<0.05) between exercised and non-exercised arms for the derived central systolic and mean arterial blood pressures. CONCLUSION: Despite similar central haemodynamic responses to the identical bouts of exercise, AI and well as central systolic and mean arterial blood pressures derived from applanation tonometry at the peripheral radial artery were statistically different when assessed at the exercising arm versus the non-exercising arm. Changes in vascular tone with exercise may modify the intrinsic characteristics of the vessel wall and could compromise the assumptions underlying transfer functions used to derive central measures using applanation tonometry.

The impact of exercise on derived measures of central pressure and augmentation index obtained from the SphygmoCor device

The purpose of this study was to investigate whether measures derived from the SphygmoCor device and its associated transfer function are influenced by exercise-induced alterations in vascular tone. Measurements were taken from either the exercised or the contralateral nonexercised limb during repeated and identical incremental hand-grip protocols. Eight male subjects performed three 3-min bouts of hand-grip exercise on two occasions. The exercise intensities were set at 3 kg, 5 kg, with a final 1.5-kg bout performed during cuff ischemia (1.5Isch). Blood pressure waveforms were recorded from the radial artery of either the exercised or nonexercised limb using applanation tonometry (SphygmoCor) during a 90-s rest period immediately after each exercise bout. Central blood pressures and augmentation indexes (AIx), an index of arterial stiffness, were derived using the peripheral waveform and the inbuilt SphygmoCor transfer function (TF). AIx was consistently approximately 10% higher in the exercised arm during all trials compared with the nonexercised limb. Similarly, there was a consistent and significant difference ( approximately 3 mmHg; P < 0.05) between exercised and nonexercised arms for the derived central systolic and mean arterial blood pressures. Despite identical bouts of exercise, AIx and central systolic and mean arterial blood pressures derived from applanation tonometry at the peripheral radial artery were statistically different when assessed at the exercising arm vs. the nonexercising arm. Changes in vascular tone with exercise may modify the intrinsic characteristics of the vessel wall and could compromise the assumptions underlying transfer functions used to derive central measures using applanation tonometry.

The effect of changing limb position on the validity of venous occlusion plethysmography

Venous occlusion plethysmography (VOP) is a technique used for the non-invasive measurement of limb blood flow. A fundamental technical consideration of venous occlusion plethysmography is that the limb in question must be placed above heart level. However, in light of advances in technology and methodology, the necessity of this has been questioned. We investigated the validity of the VOP technique with the forearm approximately 10 cm above and below the level of the heart in both resting and dynamic conditions. Nine healthy male participants performed four bouts of handgrip exercise, two at each of 15% and 30% maximum voluntary contraction (MVC) (one above and one below the heart). As hypothesized, resting forearm blood flow (FBF) measured below the level of the heart was significantly lower than for above the heart (p = 0.046). However, the opposite occurred during exercise, where FBF measured after the fifth minute of handgrip contractions was significantly higher below the level of the heart (p = 0.013). Furthermore, the ability to accurately quantify FBF below the level of the heart was severely impeded by artifact, and as such VOP appears to remain constricted to use above the phlebostatic level.

Peripheral circulatory factors limit rate of increase in muscle O(2) uptake at onset of heavy exercise.

We used an exercise paradigm with repeated bouts of heavy forearm exercise to test the hypothesis that alterations in local acid-base environment that remain after the first exercise result in greater blood flow and O(2) delivery at the onset of the second bout of exercise. Two bouts of handgrip exercise at 75% peak workload were performed for 5 min, separated by 5 min of recovery. We continuously measured blood flow using Doppler ultrasound and sampled venous blood for O(2) content, PCO(2), pH, and lactate and potassium concentrations, and we calculated muscle O(2) uptake (VO(2)). Forearm blood flow was elevated before the second exercise compared with the first and remained higher during the first 30 s of exercise (234 +/- 18 vs. 187 +/- 4 ml/min, P < 0.05). Flow was not different at 5 min. Arteriovenous O(2) content difference was lower before the second bout (4.6 +/- 0.9 vs. 7.2 +/- 0.7 ml O(2)/dl) and higher by 30 s of exercise (11.2 +/- 0.7 vs. 10.8 +/- 0.7 ml O(2)/dl, P < 0. 05). Muscle VO(2) was unchanged before the start of exercise but was elevated during the first 30 s of the transition to the second exercise bout (26.0 +/- 2.1 vs. 20.0 +/- 0.9 ml/min, P < 0.05). Changes in venous blood PCO(2), pH, and lactate concentration were consistent with reduced reliance on anaerobic glycolysis at the onset of the second exercise bout. These data show that limitations of muscle blood flow can restrict the adaptation of oxidative metabolism at the onset of heavy muscular exertion.