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Salvatore, S.S.;  Zelenski, K.N.;  Perkins, R.K. Aging and Muscle Oxygen Utilization. Encyclopedia. Available online: https://encyclopedia.pub/entry/29972 (accessed on 02 June 2024).
Salvatore SS,  Zelenski KN,  Perkins RK. Aging and Muscle Oxygen Utilization. Encyclopedia. Available at: https://encyclopedia.pub/entry/29972. Accessed June 02, 2024.
Salvatore, Sabrina S., Kyle N. Zelenski, Ryan K. Perkins. "Aging and Muscle Oxygen Utilization" Encyclopedia, https://encyclopedia.pub/entry/29972 (accessed June 02, 2024).
Salvatore, S.S.,  Zelenski, K.N., & Perkins, R.K. (2022, October 18). Aging and Muscle Oxygen Utilization. In Encyclopedia. https://encyclopedia.pub/entry/29972
Salvatore, Sabrina S., et al. "Aging and Muscle Oxygen Utilization." Encyclopedia. Web. 18 October, 2022.
Aging and Muscle Oxygen Utilization
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This entry is adapted from the peer-reviewed paper 10.3390/jfmk7040087

The cardiovascular and skeletal muscle systems are intrinsically interconnected, sharing the goal of delivering oxygen to metabolically active tissue. Deficiencies within those systems that affect oxygen delivery to working tissues are a hallmark of advancing age. Oxygen delivery and utilization are reflected as muscle oxygen saturation (SmO2) and are assessed using near-infrared resonance spectroscopy (NIRS). SmO2 has been observed to be reduced by ~38% at rest, ~24% during submaximal exercise, and ~59% during maximal exercise with aging (>65 y).

aging muscle oxygen saturation (SmO2) near-infrared resonance spectroscopy (NIRS) muscle metabolism Exercise

1. Introduction

The population of older adults is expanding due to greater life expectancy by means of advancements in medical technology and a more comprehensive understanding of physiological processes. By the year 2030, there is an expected 44% increase in the population of individuals aged 65 and older [1]. However, length of life increases the susceptibility for age-related diseases. As a result, individuals aged ~75 y and older contribute to about two-thirds of the annual 868,662 cardiovascular disease-related deaths [2][3]. Currently, the financial burden associated with cardiovascular disease is USD 555 billion annually and is expected to increase to USD 1.1 trillion by 2035 [4]. Beyond the influence of cardiovascular disease in clinical health, a robust cardiovascular system is also critical to aerobic fitness and exercise performance. More specifically, the cardiovascular system is essential for the delivery of oxygen to meet the metabolic demand of tissues. This requirement is increased during aerobic activity, as working muscles can use as much as 85% of the oxygen that is delivered [5][6][7]. With advancing age, the ability to meet increased metabolic demand gradually becomes more difficult due to the progressive decline in aerobic fitness. The rate of decline in aerobic fitness can be as much as ~1% per year following 30 years of age [8].
Working muscles require a greater supply of oxygen to withstand increased metabolic demand. Oxygen levels are measured within skeletal muscle tissue by determining the muscle oxygen saturation (SmO2), depicting the balance between oxygen delivery and consumption [9]. Oxyhemoglobin (O2Hb) and deoxyhemoglobin (HhB) are each assessed to calculate total hemoglobin (O2Hb + HhB = ThB) and are typically expressed as a percentage (([O2Hb/ThB]) × 100) = %SmO2 [10][11]. Measurements of SmO2 are generally obtained via near-infrared resonance spectroscopy (NIRS) [10], which has been modified from its original use to assess local SmO2 and blood flow in a muscle of interest at rest, during exercise, and into recovery. Through the use of this device, insight into the overall age-related reduction in oxygen delivery, utilization, and extraction by skeletal muscle can be gained [12][13][14].
Coinciding with the decline in whole-body oxygen utilization with age (i.e., VO2max), studies leveraging NIRS technology have shown similar age-related changes in local skeletal muscle oxygen utilization. Along the continuum from rest to maximal exercise and into recovery, it has been identified that aging reduces local oxygen availability. As age progresses, a variety of factors likely contribute to impairments in the oxygen delivery and utilization cascade, resulting in reductions in SmO2 at rest [13][15][16] during aerobic exercise [13][15][16][17][18][19], and prolonging restoration of metabolic homeostasis following exercise [12][15][20][21]. Impaired SmO2 may be attributed to lower muscle mass [22][23], insufficient blood flow [24][25], decreased capillary supply and function [26], dysfunctional endothelial cells [27][28], decreased nitric oxide production [28][29], and decreased mitochondrial content and function [30][31][32]. Although there are many potential factors that decrease local SmO2, mismanagement of reactive oxygen species (ROS) is suspected to be a major contributor to each of those components within the oxygen delivery cascade. More specifically, the overproduction and insufficient scavenging of ROS are underlying catalysts for decreases in whole-system function, which is exacerbated with advancing age [33]. Therefore, it is likely that damage observed at the level of the tissue is a primary effect of aging and a consequence of excess ROS mismanagement.
Cardiovascular and skeletal muscle function are intrinsically interconnected due to the interface at the cellular level. Together, these systems form a complex network that relies on effective communication to manage oxygen delivery, extraction, and utilization in skeletal muscle. Multiple reports over the last several years have identified age-related alterations in muscle oxygen utilization that serve as potential explanations for reduced exercise capacity with advanced age. Given that these metabolic processes are critical to maintain optimal health and exercise performance, the purpose of the researchers is to synthesize and provide an update on the current state of the literature regarding the effects of aging in apparently healthy individuals and muscle oxygen utilization.

2. Aging and Muscle Oxygen Utilization

The cardiovascular and skeletal muscle systems, although distinct in their specific system tasks, share the joint responsibility of meeting metabolic demand. To accomplish this, these systems cooperate to supply adequate oxygen to working muscles. Overall, the assessment of oxygen supply and utilization at the level of the tissue (i.e., SmO2) has revealed an apparent primary effect of aging. In fact, healthy aging (>65 y) reduces SmO2 at rest (~38%), during submaximal (~24%) and maximal (~59%) exercise [13][15]. In addition, the time required for SmO2 restoration following exercise in older adults dramatically exceeds that of their younger counterparts [13][15]. It is essential that the cardiovascular and skeletal muscle systems respond quickly to meet changes in metabolic demand. However, the inability to meet current demand may indicate that one or more components involved in the oxygen delivery cascade are impaired.

2.1. Submaximal Exercise

In general, there is an inverse relationship between SmO2 and exercise intensity in healthy individuals, both young and older. More specifically, SmO2 decreases in response to increasing exercise intensity. However, this effect appears to be more pronounced due to the aging process. SmO2 has been shown to be better maintained in 25 y (~73%) than 73 y individuals (~64%) at the same absolute cycling workload (i.e., 50 W) [15]. In this same study, SmO2 continued to decrease similarly in both groups as intensity increased to 75 W (young: ~60%; older: ~54%). Interestingly, age-related differences in SmO2 are still present as exercise is reported in relative terms. At 50% of maximal workload, younger individuals exhibit a greater SmO2 than their older counterparts (young: ~68%; older: ~58%). Disparity in SmO2 between groups was maintained as relative exercise intensity increased to 75% of the max (younger: ~63%; older: ~55%). It is important to note that the rate of decrease in SmO2 was greater between rest and 50% than between 50 and 75% of the maximal workload for both groups.
There appears to be a muscle-specific effect of exercise on SmO2 [16][19], potentially due to differences in fiber type and unequal distribution of blood within muscle [19][34][35]. During submaximal cycling from rest to 120 watts, older adults (~65 y) display lower SmO2 in the rectus femoris (RF), biceps femoris (BF), gastrocnemius lateralis (GL), tibialis anterior (TA) and distal portion of the vastus lateralis (VLd) than younger adults (~23 y) [16]. However, SmO2 in the proximal end of the vastus lateralis (VLp), vastus medialis (VM) and the gastrocnemius medialis (GM) does not appear to be affected by aging at rest or during submaximal exercise. Variances in SmO2 may be attributed to distinctions in actions of specific muscles as well as differences in muscle perfusion, oxygen consumption and dependent upon fiber type composition between different muscles or within the same muscle [16][36]. In support, it has been suggested that there are disparities in the rate of atrophy between muscle fiber types, with type II fibers appearing to be more affected with advancing age [37][38].
The aging process appears to alter VO2 kinetics during phase II [18], known as the primary or metabolic phase in which pulmonary VO2 rapidly increases until a steady state is met. During phase II, pulmonary VO2 closely reflects muscle VO2 profiles [17][39][40][41]. This effect was explored by analyzing muscle deoxygenation (Hhb) at the onset of moderate-intensity exercise between older (~68 y) and younger adults (~25 y) with a heavy intensity warm-up (HWU) and without a warm-up (NWU). The key finding from this study related to SmO2 demonstrates that a HWU is necessary to prime muscle metabolic processes. The authors report that the time delay before an NIRS-derived increase in deoxygenated Hhb signal was significantly longer following a HWU in the older (HWU: ~34 s vs. NWU: ~22 s), but not the younger group (HWU: ~21 s vs. NWU: ~25 s). The slower response of deoxygenated Hhb signals in older adults following HWU is considered favorable, suggesting that oxygen delivery is increasing at a faster rate than oxygen utilization. In addition, the slowed rate of Hhb signifies improved adjustments in local muscle perfusion and oxygen delivery at the onset of a subsequent moderate-intensity exercise, faster adaptation of VO2 kinetics, and decreases the effects of accelerated hypoxia that occurs at the onset of exercise, which are more difficult to adjust to with advancing age.
Similarly, other studies have demonstrated an impact of a HWU prior to submaximal exercise on whole body and local oxygen utilization in older adults (>66 y) [17]. Exercise intensity was set at 80% of each individual’s first ventilatory threshold (VT1). Results indicated the group that completed a HWU before submaximal exercise responded more favorably than the group that did not perform a warm-up. The group that performed a HWU had ~12% reduction in pulmonary and local muscle oxygen deficit during that trial than the group that did not perform a warm-up. Additionally, the rate of adjustment in pulmonary VO2 also increased following the HWU trial. This was reflected as the effective time constant (τ’) (~39 s vs. ~36 s) in oxidative metabolism, with the time constant representative of the amount of time it takes for the body’s systems to react to a shift in workload [42]. Furthermore, at VT1, the HWU group exhibited a lower respiratory exchange ratio than the NWU group (NWU: ~0.97 vs. HWU: ~0.91). Collectively, HWU appears to prime metabolic functions for improved oxygen delivery and utilization in aging individuals.

2.2. Maximal Exercise

Muscle oxygen saturation has also been shown to decrease at maximal exercise with aging. Study of healthy older (~67 y) and younger (~27 y) individuals demonstrates that aging reduces SmO2 by up to ~59% during maximal cycle exercise [13]. While SmO2 progressively decreases as a result of increasing exercise intensity in a somewhat similar fashion between younger and older individuals, the older individuals exhibited substantially lower SmO2 than their younger counterparts from baseline to maximal exercise. At maximal exercise, SmO2 levels were significantly lower in the older compared to the younger individuals (older: ~28% vs. younger ~51%). In support, muscle oxygen saturation at peak exercise has also been reported to be lower in older (~73 y) than younger adults (~25 y) [15]. At peak exercise, Δoxy-Hb/Mb (i.e., an indicator of the balance between oxygen supply and utilization) in the older adults was significantly lower than in the younger population (approximately −6 μmol/L vs. 0 μmol/L). This indicates that the relative concentrations of oxygenated hemoglobin/myoglobin are reduced in the aging population.

2.3. Recovery Time

Recent findings have indicated prolonged recovery time following exercise in older individuals. To evaluate this effect, recovery times were compared following a ramp cycle test to exhaustion among healthy older (OA; ~73 y), middle-aged (MA; ~50 y), and younger adults (YA; ~25 y). The authors found a hierarchical recovery pattern following exercise (OA: ~42 s > MA: ~25 s > YA: ~22 s) [15]. These findings demonstrated that older adults had ~51% longer recovery times than middle-aged adults and ~63% longer than younger adults. In contrast, there were no statistical differences in muscle oxygen dynamics during submaximal exercise between MA and YA. Therefore, muscle oxygen metabolism may be preserved in the early stages of aging and progressively exacerbated in the latter stages.
In support of prolonged restoration of SmO2 following aerobic exercise, it has been shown that age and exercise training status as well as the combination of both factors impact recovery time [21]. Recovery time among four groups of middle- and older-aged women were analyzed following maximal cycling exercise. Active middle-aged (AM; ~53 y), active older (AO; ~67 y), sedentary middle-aged (SM; ~50 y), and sedentary older (SO; ~66 y) women were evaluated to determine the time required to re-establish 50% SmO2 between resting and exhaustion levels (T½ reoxy). Results indicated that a hierarchical pattern in the recovery of SmO2 following maximal exercise occurred (SO: 46 s > SM: 36 s > AO: 30 s > AM: 23 s). This corresponds to AO having ~27% slower T½ reoxy time than AM, SO having ~25% slower T½ reoxy time than SM, and SO having ~43% slower T½ reoxy time than AO. These data suggest there is a primary effect of aging on muscle reoxygenation; however, habitual physical activity may slow this effect.
Most studies have assessed SmO2 recovery in the lower extremities; however, analysis of SmO2 recovery in muscles of the forearm show this region is also affected with advancing age. Forearm muscles were examined in healthy younger (~34 y), healthy older (~67 y), and older adults at risk for CVD (~67 y) to assess the reoxygenation time following handgrip exercise performed at 30% maximal voluntary contraction (MVC) [20]. Handgrip exercises were performed at 60 contractions per minute, 0.5 s contraction/0.5 s relaxation until volitional exhaustion. Muscle oxygen saturation recovery over the first five seconds following exercise termination (SmO2RR) was significantly faster in the healthy young group (~1.65 %/s) compared to the healthy older group (~0.92%/s). Furthermore, the older at-risk for CVD group exhibited the slowest SmO2RR (~0.45%/s). The younger group restored oxygen ~57% faster than the healthy older group and ~114% faster than the at-risk for CVD group, respectively. However, no statistical differences were observed between the older groups.
Similarly, analysis of forearm SmO2 recovery was performed while utilizing a series of rapid arterial cuff occlusions performed following handgrip exercise at 50% MVC until SmO2 decreased by ~50% (~10–30 s), at which point oxygen utilization and mitochondrial function in the flexor digitorum profundus of the forearm were analyzed [12]. After exercise cessation, a series of rapid cuff inflations were employed to generate a muscle oxygen consumption mVO2 recovery curve [12]. By measuring SmO2 during this protocol and inputting values into a previously established mVO2 recovery equation [43][44][45], results indicated that older adults (~72 y) had ~33% longer (~52 s vs. ~37 s) post-exercise mVO2 recovery kinetics (i.e., mitochondrial function) compared to their younger counterparts (~25 y).

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Subjects: Endocrinology & Metabolism
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register :
Sabrina S. Salvatore
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Kyle N. Zelenski
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Ryan K. Perkins
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Update Date: 19 Oct 2022
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