Nelson, NL. Breast cancer-related lymphedema and resistance exercise: a systematic review. J Strength Cond Res 30(9): 2656-2665, 2016-Breast cancer-related lymphedema (BCRL) is characterized by the accumulation of fluid in the interstitial tissues in the arm, shoulder, neck, or torso and attributed to the damage of lymph nodes during breast cancer treatments involving radiation and axillary node dissection. Resistance exercise training (RET) has recently shown promise in the management of BCRL. The aims of this review were twofold: (a) To summarize the results of recent randomized controlled trials (RCTs) investigating the effect of resistance exercise in those with, or at risk for, BCRL. (b) To determine whether breast cancer survivors can perform RET at sufficient intensities to elicit gains in strength without causing BCRL flare-up or incidence. A search was performed on the electronic databases PubMed, MEDLINE, SPORT Discus, and Science Direct, up to July 10, 2015, using the following keywords: breast cancer-related lymphedema, strength training, resistance training, systematic review, and breast cancer. Manual searches of references were also conducted for additional relevant studies. A total of 6 RCTs, involving 805 breast cancer survivors, met the inclusion criteria and corresponded to the aims of this review. The methodological quality of included RCTs was good, with a mean score 6.8 on the 10-point PEDro scale. The results of this review indicate that breast cancer survivors can perform RET at high-enough intensities to elicit strength gains without triggering changes to lymphedema status. There is strong evidence indicating that RET produces significant gains in muscular strength without provoking BCRL.

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Although exercise-associated muscle cramps (EAMC) are highly prevalent among athletic populations, the etiology and most effective management strategies are still unclear. The aims of this narrative review are 3-fold: (1) briefly summarize the evidence regarding EAMC etiology; (2) describe the risk factors and possible physiological mechanisms associated with neuromuscular fatigue and EAMC; and (3) report the current evidence regarding prevention of, and treatment for, EAMC. Based on the findings of several large prospective and experimental investigations, the available evidence indicates that EAMC is multifactorial in nature and stems from an imbalance between excitatory drive from muscle spindles and inhibitory drive from Golgi tendon organs to the alpha motor neurons rather than dehydration or electrolyte deficits. This imbalance is believed to stem from neuromuscular overload and fatigue. In concert with these findings, the most successful treatment for an acute bout of EAMC is stretching, whereas auspicious methods of prevention include efforts that delay exercise-induced fatigue. Muscle Nerve 54: 177-185, 2016.

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